19 research outputs found
In thrombin stimulated human platelets Citalopram, Promethazine, Risperidone, and Ziprasidone, but not Diazepam, may exert their pharmacological effects also through intercalation in membrane phospholipids in a receptor-independent manner
Intercalation of drugs in the platelet membrane affects phospholipid-requiring enzymatic processes according to the drugs’ intercalation capability. We investigated effects of Promethazine, Citalopram, Ziprasidone, Risperidone, and Diazepam on phospholipase A2 (PLA2) and polyphosphoinositide (PPI) metabolism in thrombin-stimulated human platelets. We also examined effects of the drugs on monolayers of glycerophospholipids using the Langmuir technique. Diazepam did not influence PLA2 activity, had no effects on PPI cycle, and caused no change in mean molecular area of phospholipid monolayers. The remaining psychotropic drugs affected these parameters in different ways and levels of potency suggesting that they act by being intercalated between the molecules of adjacent membrane phospholipids, thus causing changes in substrate availability for phospholipid-hydrolyzing enzymes (PLA2 and Phospholipase C). We show that several psychotropic drugs can also have other cellular effects than receptor antagonism. These effects may be implicated in the psychotropic effects of the drugs and/or their side effects
Systematic review regarding metabolic profiling for improved pathophysiological understanding of disease and outcome prediction in respiratory infections
Effect of n-butanol and cold pretreatment on the cytoskeleton and the ultrastructure of maize microspores when cultured in vitro
Adenine Nucleotide and Adenosine Metabolism in Cultured Coronary Endothelial Cells: Formation and Release of Adenine Compounds and Possible Functional Implications
Intraplatelet serotonin in patients with diabetes mellitus and peripheral vascular disease
Immunological localisation of beta-thromboglobulin and platelet factor 4 in human megakaryocytes and platelets.
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Mathematical techniques for understanding platelet regulation and the development of new pharmacological approaches
Mathematical and computational modeling is currently in the process of becoming an accepted tool in the arsenal of methods utilized for the investigation of complex biological systems. For some problems in the field, like cellular metabolic regulation, neural impulse propagation, or cell cycle, progress is already unthinkable without use of such methods. Mathematical models of platelet signaling, function, and metabolism during the last years have not only been steadily increasing in their number, but have also been providing more in-depth insights, generating hypotheses, and allowing predictions to be made leading to new experimental designs and data. Here we describe the basic approaches to platelet mathematical model development and validation, highlighting the challenges involved. We then review the current theoretical models in the literature and how these are being utilized to increase our understanding of these complex cells