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Biomedical subjects

J L Gordon

Publications and source records attributed to J L Gordon.

At least 91 records · Page 5Linked to original sources
PubMed1978

Interaction of leukocytes with vascular cells in culture.

The nature, kinetics and cofactor requirements of leukocyte adhesion to cultured vascular cells have been investigated in vitro, using a model system in which leukocyte suspensions are in continuous motion over the cultured cells. Adhesion is assessed by histological examination or by using 51Cr-labelled leukocytes. Leukocytes adhere preferentially to endothelial cell monolayers rather than to smooth muscle cells, adventitial fibroblasts or serum-coated glass. Arterial and venous endothelium are equally good substrates for leukocyte adhesion, and lymphocytes and granulocytes at the same suspension density adhere to endothelial cells in similar numbers. Adherence is greatest during the first 10 min, and is inversely related to flow rate. Numbers of leukocytes adhering to the cell monolayer are proportional to the initial concentration of leukocytes in suspension, although only 2--10% of the leukocytes adhere. Leukocytes that have adhered to the cell monolayer spread over the cells and then migrate, apparently through intercellular junctions. Adhesion requires Ca2+ or Mg2+ ions, but not plasma protein cofactors. Fewer leukocytes adhere to endothelial cells grown for 48 h in rapidly stirred medium than to cells grown under conventional, static conditions.

Blood Vessels↗
PubMed1977

Endotoxin-induced platelet aggregation and secretion. I. Morphological changes and pharmacological effects.

Endotoxin lipopolysaccharide (LPS) from Acinetobacter 199A induced aggregation of blood platelets from immune adherence-positive species (rat, rabbit) but not from immune adherence-negative species such as pig and man. Aggregation occurred in 2 phases: the first was not accompanied by secretion of platelet constituents, was apparently a consequence of C3 activation, and was selectively inhibited by EGTA. The second phase of aggregation was associated with secretion of platelet granule contents, and with a lesser amount of cytoplasmic leakage. Secondary aggregation was abolished by the sulphydryl alkylating agent N-ethylmaleimide, and by agents which increased the level of cyclic AMP in platelets, such as prostaglandin E1 (a stimulator of adenylate cyclase) and methyl xanthines (inhibitors of phosphodiesterase). Secondary aggregation was partly inhibited by agents which block platelet prostaglandin biosynthesis (e.g. aspirin, indomethacin). Primary aggregation was unaffected by these inhibitors at concentrations which blocked secondary aggregation.

Acetylglucosaminidase↗
PubMed1977

Endotoxin-induced platelet aggregation and secretion. II. Changes in plasma membrane proteins.

Responses of blood platelets to bacterial endotoxin lipopolysaccharide (LPS) have been correlated with changes in the molecular organization and composition of the platelet plasma membrane proteins. Binding of LPS, which occurred in the absence of Ca2+, was distinguished from platelet aggregation and degranulation, which required Ca2+ and plasma proteins. Changes in membrane organization were detected by double-labelling with [125I] and [131I] iodide, mediated by lactoperoxidase and hydrogen peroxide. Changes in total membrane composition were detected by gel electrophoresis of isolated membranes. Binding of LPS was associated with increased accessibility of a protein of mol. wt. 80000 to iodination. After aggregation and degranulation there was, in addition, increased accessibility of proteins of mol. wt. 68000 and 48000. Isolated membranes from LPS-stimulated platelets contained more of a protein of mol. wt. 200000 and less of a protein of mol. wt. 220000 than control membranes prepared from unstimulated platelets in the presence of cAMP and aminophylline. The relationship of the modified plasma membrane proteins to the contractile proteins of the platelet and their possible redistribution in the cell during aggregation and secretion is discussed.

Acinetobacter↗
PubMed1977

Endothelial adenine uptake as an assay for cell- or complement-mediated cytotoxicity.

[3H] Adenine uptake by monolayers of cultured pig aortic endothelium was characterized and used as the basis for a terminal adenine uptake cytotoxicity assay. This assay was used to demonstrate specific cytotoxicity against donor-type endothelium by serum and by peripheral blood lymphocytes from skin-graft allergized pigs, and to compare the time course of these two types of effector mechanism.

Adenine↗
PubMed1976

Platelet-aggregating activity of type I and type III collagens from human aorta and chicken skin.

Human or chicken type III collagen dissolved in 0.1 M-acetic acid was much more potent than type I collagen at inducing platelet aggregation. After incubation in 0.38M-Na2HPO4 to promote fibrillogenesis, the platelet-aggregating activity of both collagen types increased, and type I was then virtually equiactive with type III. Preincubation in cell-free plasma increased the activity of chicken but not that of human collagen. The platelet-aggregating activity of type III collagen did not appear to depend on the integrity of the intrachain disulphide bonds.

Adult↗
PubMed1976

Uptake of 5-hydroxytryptamine by rat blood platelets and its inhibition by adenosine 5'-diphosphate.

1 The uptake of 5-hydroxytryptamine (5-HT) by rat blood platelets in citrated plasma was linear for at most 10 s and was substantially complete within 3 minutes. 2 Adenosine 5'-diphosphate (ADP) was a potent inhibitor of 5-HT uptake (Ki=0.38 muM) and kinetic analysis revealed that the inhibition was not competitive. 3 Inhibition of 5-HT uptake by ADP was abolished in the presence of prostaglandin E1 and 2-n-amylthio-AMP, which also inhibit the stimulant actions of ADP on blood platelets. 4 It is concluded that ADP could inhibit 5-HT uptake by changing the Na+/K+ distribution across the cell membrane, and the biological significance of this is discussed.

Adenosine Diphosphate↗