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Titlebook: Renal Eicosanoids; Michael J. Dunn,Carlo Patrono,Giulio A. Cinotti Book 1989 The Editor(s) (if applicable) and The Author(s), under exclus

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The Cell Biology of Fibroblast Cyclooxygenase,a in studies with human dermal fibroblast cultures to immunoprecipi-tate selectively the COX enzyme. Labeling of the cells with [.S]-methionine, solubilization of cellular COX followed by its immunoprecipitation, SDS-PAGE electrophoresis and fluorography enabled us to determine directly the syntheti
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Arachidonic Acid Metabolism During Interactions Between Glomerular and Bone Marrow-Derived Cells,ies in which platelets and blood vessels were coincubated and AA metabolites were analysed. Over subsequent years most of the researchers in this field focused their interest on the interaction between either endothelium and platelets, polymorphonuclear leukocytes (PMNL) and platelets, or PMNL and e
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The Renal Cytochrome P450 System Generates Novel Arachidonic Acid Metabolites,d AA from cellular lipids. Once liberated from membrane lipids by diverse stimuli (peptide hormones, neurotransmitters and mechanical disruption), the free AA is rapidly metabolized. Metabolism of AA involves three pathways: (a) cyclooxygenase, leading to the formation of prostaglandins, thromboxane
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Peptide Hormones, Cytosolic Calcium and Renal Epithelial Response,peptide hormones, neurotransmitters and growth factors are fundamental to understanding how the signals mediated by circulatory substances, which interact with cell surface receptors, produce their effects intracellularly. The cellular responses to a wide variety of signal molecules are somewhat lim
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Prostaglandins, Thromboxane and Leukotrienes in the Control of Mesangial Function,ort of contraction of cultured rat mesangial cells by the vasoactive peptides, angiotensin II (ANG II) and arginine vasopressin (AVP) (2,4), considerable interest focused on the hypothesis that mesangial cells may regulate glomerular blood flow and filtration in synergism with afferent and efferent
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Eicosanoids and Platelet Activating Factor as Possible Mediators of Injury in Experimental Nephropaal expression of toxic or immune-mediated nephropathies has been the subject of extensive investigations in the last few years. More recently the demonstration that, beside circulating inflammatory cells, resident renal cells can generate prostaglandins and thromboxane A. (TxA.) (1,2) as well as PAF
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