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Biomedical subjects

A Stier

Publications and source records attributed to A Stier.

At least 73 records · Page 4Linked to original sources
PubMed1975

Titrating dietary linoleate to in vivo platelet function in man.

Platelet aggregation time significantly increased within 48 hours in response to an increase in dietary linoleate of 4% of calories while disaggregation time decreased significantly in 96 hours. A change as small as 0.5% of calories was associated with significant alterations within 4 days. In this group, dietary linoleate appears to be related to platelet function by the equations Aggregation time equals 41.14 plus 2.79 linoleate Disaggregation time equals 11.04 minus 25.52 linoleate.

Adult↗
PubMed1975

Beneficial effect of increased dietary linoleate upon in vivo platelet function in man.

The effect of increasing dietary linoleate upon in vivo platelet aggregation and disaggregation in 20 males and 46 female adult humans was studied. In creasing exogenous linoleate for 2 weeks from 2.89 +/- 0.11 to 5.00 +/- 0.26% of energy was associated with the doubling of the aggregation time and halving of the disaggregation time. Decreasing dietary linoleate in the following 2-week feeding period was associated with a reversal of the effect.

Aged↗
PubMedDate not supplied

Direct visualization of a cardiolipin-dependent cytochrome P450scc-induced vesicle aggregation.

Cytochrome P450scc can be reconstituted successfully into large unilamellar phospholipid vesicles by a combined octylglucoside dialysis/adsorption method. Freeze-fracture electron microscopy was used to analyze the morphology, distribution, and protein topology of the cytochrome P450scc vesicles in dependence on lipid composition. Particles were observed only in close contact to the vesicle surface, probably representing tightly associated cytochrome P450scc at the outer vesicle surface. In cytochrome P450scc vesicles similar in lipid composition to the inner membrane of bovine mitochondria direct evidence by freeze-fracturing was found for a specific cytochrome P450scc-induced aggregation of the vesicles. The vesicle aggregation critically depends on the content of the specific mitochondrial membrane constituent cardiolipin. The aggregation and thus the intervesicular contacts were observed to be inhibited by both addition of anti-cytochrome P450scc IgG and adrenodoxin. Enzymatic reduction of cytochrome P450scc in the liposomal membrane by its electron transfer partners completely indicates an asymmetrical localization in/at the outer side of the bilayer membrane. It is suggested that vesiculation of the inner mitochondrial membrane may be a consequence of the characteristic cardiolipin-dependent cytochrome P450scc membrane topology: the cardiolipin binding, peripheral, non-bilayer-spanning integration as an oligomer in the outer leaflet of the membrane may play a role in the dynamics of formation and dissociation of intramitochondrial vesicles with a functional importance for steroidogenesis.

Adrenodoxin↗
PubMedDate not supplied

Postischemic cell death in reperfused porcine hearts is not attenuated by the spin trap agent PBN during early reperfusion.

Ischemic, reperfused porcine hearts were used to investigate whether the spin trap agent PBN (N-tert-butyl-alpha-phenylnitrone) attenuates postischemic cell death by scavenging of free radicals. The left anterior descending coronary artery (LAD) was ligated distally in 16 pigs for 45 min and then reperfused for 3 h. PBN (coronary concentration approximately 1 mM) was infused into the LAD of eight pigs during the first 45 min of reperfusion. Electron spin resonance spectroscopy (ESR) was performed to identify free radical adducts in the reperfused coronary venous blood. Regional systolic shortening (SS%) was determined by sonomicrometry. Infarct size was evaluated as the percentage of infarcted (tetrazolium stain) to ischemic (dye technique) myocardium. The transmural ultrastructural degree of myocardial injury as well as myocardial ATP levels were assessed at the end of the experiment. Intracoronary treatment with PBN during early reperfusion did not attenuate myocardial damage. Infarct sizes (control group 59 +/- 19%, treated group 55 +/- 14%), transmural ultrastructural alterations, myocardial ATP concentrations (control group 1.8 +/- 0.3 mumol/mg frozen weight, treated group 1.7 +/- 0.4 mumol/mg) and regional systolic shortening at the end of the experiments (control group -1 +/- 5%, treated group -2 +/- 6% did not differ significantly. Furthermore, under various experimental conditions of spin trapping, free radical adducts could not be identified in coronary venous blood during early reperfusion. The results suggest that the spin trap agent PBN (1 mM) does not affect postischemic cell death in porcine hearts.

Adenosine Triphosphate↗