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Biomedical subjects

H Prydz

Publications and source records attributed to H Prydz.

At least 145 records · Page 8Linked to original sources
PubMed1982

Thromboplastin (factor III) activity in human monocytes induced by immune complexes.

Immune complexes induced the synthesis of apoprotein III, the protein component of tissue thromboplastin (tissue factor), in human monocytes cultured in vitro. The response was maximal (11.1 +/- 1.7 fold increase (mean +/- SEM) when immune complexes were formed at antigen/antibody equivalence. Immune complexes formed with the antigen-binding fragments (F(ab')2) of immunoglobulins induced a 4.7 +/- 1.4 fold activity increase, suggesting that another signal mechanism in addition to the Fc-receptor may be involved.

Animals↗
PubMed1982

Effect of purified protein derivative and sonicates of Mycobacterium leprae and Mycobacterium bovis BCG on thromboplastin response in human monocytes in vitro.

Human monocytes isolated from peripheral blood responded with increased thromboplastin expression upon stimulation in vitro with three mycobacterial antigens: tuberculin purified protein derivative and sonicates of Mycobacterium boviS BCG and Mycobacterium leprae. The stimulating principle of mycobacteria is probably a cell wall constituent since crude extracts of cell walls were 2.5 to 25 times more potent in stimulating thromboplastin synthesis than were whole sonicates. This thromboplastin response was inhibited by inhibitors of RNA and protein synthesis, dexamethasone, and agents that caused elevation of intracellular cyclic AMP. The presence of lymphocytes did not enhance the monocyte thromboplastin response significantly during the first 24 h of incubation. For M. bovis BCG and M. leprae sonicates, the thromboplastin response correlated with general activating effects measured by determining the release of lysozyme and beta-glucuronidase. The role of thromboplastin in chronic inflammatory reactions is discussed.

Antigens, Bacterial↗
PubMed1982

Toxicity of phospholipase C in rabbits.

Tissue thromboplastin is the most potent physiological trigger of blood coagulation and is probably involved in the pathogenesis of several forms of intravascular coagulation. Phospholipase C from Bacillus cereus is an effective inhibitor of thromboplastin. As part of an investigation into the possible use of phospholipase C as a therapeutic or prophylactic agent in thrombosis and other forms of intravascular coagulation, we have previously studied its effect in rats. We now report on the toxicity in rabbits (along with some data on cats and monkeys). Estimated LD50 for rabbits was about 0.45-0.65 mg/kg (as compared to 1.70 mg/kg for rats). No respiratory or circulatory changes were observed, but phospholipase C caused a significant increase of several plasma enzymes in rabbits.

Acid-Base Equilibrium↗
PubMed1981

Phorbol esters induce synthesis of thromboplastin activity in human monocytes.

12-O-Tetradecanoylphorbol 13-acetate (TPA), phorbol 12,13-diacetate and phorbol 12,13-didecanoate were all potent inducers of thromboplastin activity in human monocytes in vitro, whereas 4 alpha-phorbol 12,13-didecanoate and 4 alpha-phorbol had no such effect. A concomitant increase in titrable apoprotein III antigen was found (apoprotein III is the protein component of thromboplastin). The increase was inhibited by cycloheximide and actinomycin D and partly by alpha-amanitin. The increase of thromboplastin activity was therefore most likely due to synthesis de novo of apoprotein III. The response was approximately halved in the absence of serum or Ca2+. Retinol had a weak inhibitory effect, and retinoic acid was inhibitory only at concentrations that also induced signs of cytotoxicity. TPA caused an initial rise in monocyte cyclic AMP concentration of about 90-120 min duration. No increase in 45Ca2+ influx was induced over 2 h. Good correlation exists between induction of apoprotein III synthesis in monocytes in vitro and mouse skin-tumour promotion in vivo by the various phorbol derivatives. Substances inactive in tumour promotion do not induce the synthesis of apoprotein III. General activating and cytotoxic effects of TPA were monitored by determining release of lysozyme, beta-glucuronidase and lactate dehydrogenase.

Apoproteins↗
PubMed1980

Lectin stimulation of tissue thromboplastin activity in human monocytes in vitro.

Lectins (phytohaemagglutinin, concanavalin A and wheat germ agglutinin) trigger an increase in tissue thromboplastin activity of human monocytes in vitro. The presence of serum was not necessary and did not enhance the activity. The increase was inhibited by cycloheximide and actinomycin D, suggesting that de novo protein synthesis is involved.

Agglutinins↗
PubMed1979

Studies on a subcellular system for vitamin K-dependent carboxylation.

The subcellular localization of acarboxyprothrombin and the vitamin K-dependent carboxylation system has been studied using livers from vitamin K-deficient rats and found to be mainly in the membranes of the rough microsomal fraction. Bovine acarboxyprothrombin or fragment 1 thereof were inactive as substrates in the rat carboxylating system.

Animals↗
PubMed1979

The effect of aphidicolin on DNA synthesis in isolated HeLa cell nuclei.

The effect of the inhibitor aphidicolin on DNA synthesis in isolated nuclei from HeLa cells and on the activities of partially purified DNA polymerases has been tested. Aphidicolin inhibited DNA synthesis and DNA polymerase alpha very efficiently whereas DNA polymerases beta and gamma were insensitive to the drug. The results indicate that DNA polymerase alpha is the polymerase active during elongation as well as in the gapfilling process of discontinuous DNA synthesis.

Anti-Bacterial Agents↗
PubMed1979

Circulating tissue thromboplastin during hip surgery.

An immunoradiometric assay for tissue thromboplastin has been established. Blood levels in 6 patients undergoing total hip replacement have been determined. In 3 patients, high levels of circulating apoprotein III were found at various stages of the operation, showing a release of tissue thromboplastin chiefly during impaction of the prosthesis into the femoral bone. The other 3 patients had low or undetectable levels.

Adult↗
PubMed1979

Protection of pregnant mice with phospholipase C and with Arvin against foetal death induced by bacterial lipopolysaccharide.

Injection of bacterial lipopolysaccharide into pregnant mice resulted in fibrinogen accumulation, thrombosis and haemorrhage in the placental tissue and foetal death. Depletion of circulating fibrinogen by a thrombin-like enzyme from the venom of Malayan pit viper, Arvin, prevents foetal death. Foetal protection was also obtained by treating the mothers with a preparation of phospholipase C from Bacillus cereus known to inactivate tissue thromboplastin. It is suggested the lipopolysaccharide causes foetal death by inducing thrombosis as a consequence of activation of placental thromboplastin.

Ancrod↗
PubMed1978

Tissue thromboplastin activity of isolated human monocytes.

Certain agents that induce spreading of or increased content or release of lysosomal enzymes from human monocytes also induce a dramatic increase in tissue thromboplastin content of the cells. The increase is inhibited by cycloheximide and actinomycin D and does not appear in granulocyte, lymphocyte or platelet populations treated in the same way. The effect of several other substances on the development of monocyte tissue thromboplastin activity is reported.

Blood Coagulation↗
PubMed1978

NAD(P)H dehydrogenase and its role in the vitamin K (2-methyl-3-phytyl-1,4-naphthaquinone)-dependent carboxylation reaction.

A simple three-step method was established for the purification of NAD(P)H dehydrogenase (quinone) ('DT-diaphorase', EC 1.6.99.2) from rat liver by affinity chromatography with a recovery of above 50%. The final enzyme preparation was purified about 750-fold and was electrophoretically homogeneous. Gel filtration showed that the enzyme had a mol.wt. of about 55 000, and one molecule of FAD was found per 55 000 mol.wt. Sodium dodecyl sulphate/polyacrylamide-gel electrophoresis gave a mol.wt. of about 27 000. Two N-terminal amino acids, asparagine/aspartic acid and glutamine/glutamic acid, were found in about equal yield, suggesting the presence of two non-identical polypeptide chains in the enzyme. NAD(P)H dehydrogenase was selectively removed by this affinity-chromatographic method from a microsomal carboxylation system. The system, which was solubilized by detergent and is dependent on vitamin K (2-methyl-3-phytyl-1,4-naphthaquinone or analogues with other side chains), lost its activity on the removal of the enzyme. The activity can be completely restored to the system by adding purified cytoplasmic NAD(P)H dehydrogenase or by using the quinol form of vitamin K1 (2-methyl-3-phytyl-1,4-naphthaquinol).

Animals↗
PubMed1978

The role of macrophage activation in chronic inflammation.

The macrophage is the characteristic cell type in chronic inflammatory reactions, in the rheumatoid synovium, as in other sites. When macrophages are activated, considerable synthesis of enzymes and other proteins occurs. Macrophages can be activated by (i) products of activated lymphocytes, (ii) immune complexes and (iii) the complement cleavage product C3b. Among the many consequences of macrophage activation are (i) secretion of hydrolytic enzymes, (ii) cleavage of C3 into C3a, which is cytolytic, and C3b, (iii) production of tissue thromboplastin, a powerful procoagulant, and (iv) formation of polyamine oxidase, which in the presence of appropriate substrates generates factors that lyse or limit the proliferation of tumour cells, lymphocytes and micro-organisms. The relevance of these observations to the pathogenesis of chronic inflammatory reactions is discussed.

Animals↗