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Biomedical subjects

R J Flower

Publications and source records attributed to R J Flower.

229 records · Page 13Linked to original sources
PubMed1972

Metabolism and transfer of choline in hamster small intestine.

1. The transfer and metabolism of choline was studied with sacs of everted intestine of hamster.2. Approximately half the choline transferred from the mucosal fluid may be metabolized. High voltage electrophoresis, paper chromatography and ion exchange chromatography have been used to identify this meta bolite as betaine.3. The concentration of choline and betaine together accumulating in the gut wall and serosal fluid are greater than that of choline present initially in the mucosal fluid indicating some kind of specific mechanism for choline transport.4. A detailed analysis of choline transfer suggests that the movement of choline cannot be accounted for by simple diffusion. The concentration of choline accumulating in the gut wall and serosal fluid, the inhibitory effects of hemicholinium-3 and alpha-methylglucoside on choline transfer, and the insensitivity of betaine transfer to hemicholinium-3 suggest a specific active transport process for choline independent of active betaine transport.

Animals↗
PubMedDate not supplied

Biosynthesis of prostaglandins.

The generation of prostaglandins is catalyzed by a membrane-bound multienzyme complex. The first reaction of the biosynthetic sequence is the generation (by the enzyme 'fatty acid cyclooxygenase') of prostaglandin endoperoxides, a reaction which involves the incorporation of two moles of oxygen: this reaction probably proceeds by an ene reaction rather than a free-radical mechanism. After biosynthesis the endoperoxides can be metabolized in various ways depending on the cell-type. For example, in platelets they may be transformed into non-prostanoid compounds called thromboxanes, whereas vascular endothelium and many other tissues generate another derivative, prostacyclin. In other tissues, the 'classical' prostaglandins E, F or D may be generated. Some products of the cyclooxygenase (e.g. hydroperoxides, malonaldehyde) may have a direct toxic action on cells: prostaglandins themselves do not, but some types (especially those of the E series) are probably responsible for many of the clinical signs and symptoms of inflammation.

Cyclooxygenase Inhibitors↗
PubMedDate not supplied

The detection of lipocortins 1, 2 and 5 in central nervous system tissues from Lewis rats with acute experimental allergic encephalomyelitis.

The calcium and phospholipid-binding proteins lipocortins 1, 2 and 5 have been detected, by electrotransfer and immunoblotting techniques, in central nervous system (CNS) tissues of control Lewis rats and animals with experimental allergic encephalomyelitis (EAE). The cerebellum and spinal cord content of lipocortins 2 and 5 remained unchanged throughout the development of EAE but the amounts of the steroid-inducible protein lipocortin 1 increased in samples from pre-diseased and adjuvant-treated rats and were further enhanced in tissues from clinically sick and convalescent animals. The significance of these findings is discussed in conjunction with the ongoing changes in pathology which occur during the progression of EAE.

Acute Disease↗
PubMedDate not supplied

Recombinant human lipocortin 1 inhibits thromboxane release from guinea-pig isolated perfused lung.

The guinea-pig perfused isolated lung, used in conjunction with the cascade superfusion system to measure the release of thromboxane A2(TXA2), is a simple and convenient model for assessing the inhibition by glucocorticoids of eicosanoid formation. Dexamethasone inhibits the release of TXA2 from the lung when it is stimulated by agents such as RCS-RF2 of leukotrienes, but not when bradykinin or arachidonic acid are used. Using this model we have shown that the glucocorticoids suppress eicosanoid generation by cells through the induction of a family of phospholipase A2-inhibitory proteins now termed the 'lipocortins'. Recently the primary structure of one form of lipocortin has been elucidated and the human gene cloned. Lipocortin 1 is a polar monomeric protein with anti-phospholipase properties in vitro and we now report that when infused into guinea-pig lung preparations this protein has the same inhibitory profile as the glucocorticoids but with a more rapid onset of action. This is the first demonstration that eicosanoid formation can be inhibited by a recombinant phospholipase inhibitory protein applied extracellularly.

Animals↗