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E Wulfert

Publications and source records attributed to E Wulfert.

26 records · Page 2Linked to original sources
PubMed1985

Self-reinforcement effects: An artifact of social standard setting?

Two studies were conducted to identify mechanisms responsible for observed "self-reinforcement" effects. In Experiment 1, using a studying task, self-reinforcement procedures did not work when they were private (i.e., when others are not aware of the goals or contingencies), but did work when they were public. Self-delivery of consequences added nothing to the effectiveness of the procedure. The data suggested that public goal setting was the critical element in the procedure's effectiveness. In Experiment 2, an applied extension, goal setting alone was effective in modifying over a long time period studying behaviors of people with significant studying difficulties, but only when the goals were known to others. Overall, the two experiments make more plausible the view that self-reinforcement procedures work by setting a socially available standard against which performance can be evaluated. The procedure itself functions as a discriminative stimulus for stringent or lenient social contingencies. The application of this mechanism to other problems of applied significance is briefly discussed.

Journal Article↗
PubMed1984

Effect of lipid composition changes on carbocyanine dye fluorescent response.

Egg yolk phosphatidyl choline liposomes containing variable amounts of phosphatidyl ethanolamine, phosphatidyl inositol or phosphatidyl serine demonstrated important variations in the fluorescence of 3.3' dipropylthiodicarbocyanine. When the membrane contained no cholesterol, fluorescence was not correlated with membrane fluidity as measured by diphenyl hexatriene polarization. Increasing cholesterol concentration in valinomycin containing liposome membranes decreased the potassium induced apparent membrane potential and prevented sorption of dye to the membrane. Discontinuity in the apparent potential occurred at 30 mol% cholesterol but could not be correlated with changes in microviscosity. These results indicate that great care should be taken when correlating rapid variations of fluorescence to changes in membrane potential. We propose that changes in phospholipid metabolism could well explain fluorescent changes when monitoring the fluorescence of cyanine dye molecules sorbed to biological membranes.

Benzothiazoles↗
PubMed1984

Determination of apoprotein B in the skin.

To determine the origin of cutaneous cholesterol a method has been developed for extracting and determining by electro-immuno-assay apoprotein B in the skin as already performed by Hoff at the arterial level. This study demonstrated the presence of apoprotein B in the skin and its quantification. The easy and reliable technique employed required only conventional laboratory instruments. Repeatability and reproducibility studies give encouraging results comparable with those obtained on arterial tissue. They show that at least one part of skin cholesterol originates in low density lipoproteins.

Apolipoproteins↗
PubMed1982

Skin cholesterol and skin apoprotein B in atherosclerosis.

In order to quantify the accumulation of apoprotein B in skin we determined the amount of apo B in the skin of atherosclerotic patients using a modified Hoff's method with extraction and electroimmunoassay. Skin biopsies were taken from the lower limbs of nineteen male patients with arteriosclerosis obliterans during revascularization and from the thoracic region of thirty male patients with ischemic heart disease during coronary bypass graft surgery and thirty one male patients with abnormalities of cardiac valves during valvuloplasty. A significant positive correlation between skin apo B and skin cholesterol was found in three groups. Our data support the hypothesis that cholesterol deposit in the skin of patients with atherosclerosis is derived from plasma lipoprotein B and that the content of skin lipids parallels with the development of atherosclerosis in man.

Apolipoproteins↗
PubMed1981

Inhibition of membrane-bound hepatic 3 hydroxy-3 methyl glutaryl CoA reductase as the consequence of altered membrane fluidity.

The activity of hydroxy methyl glutaryl-CoA reductase in microsomes from rat and from human liver was inhibited in a non-competitive manner by fenofibric acid. High affinity of the microsomal preparation for the ligand allowed a one-step purification of the microsomal enzyme preparation, using a Sepharose gel coupled to the phenol analogue of fenofibric acid. Ther Arrhenius plots of partially purified hydroxy methyl glutaryl-CoA reductase in the microsomal fraction from rat liver showed that the break in the activation energy at 11 degrees C was abolished by the ligand. The results in the present study may be consistent with a modulation of membrane-bound HMG-CoA reductase activity.

Animals↗
PubMed1978

[Effect of various 2-methyl-(4'-chlorobenzoyl)-4-phenoxy)-2 propionic acid (LF 153) analogs on the respiratory activity of rat liver mitochondria].

Seven analogs of methyl-2 [chloro-4' benzoyl)-4 phenoxy]-2 propionic acid, (LF 153) have been tested for their effects on respiration and phosphorylation of rat liver mitochondria suspensions. They differ from one another by the sort of binding between both aromatic cycle as well as by the nature and position of the halogenated substitutions and alpha methylation in the propionic chain. All the compounds which have been tested acted as inhibitors of the electron transport chain and uncouplers of phosphorylations.

Animals↗