Spatial arrangement of facial nerve fibres.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to A White.
Explore the source record for details and available documents.
The effects of metabolic inhibitors and carbohydrates on histamine release induced by human leukocyte lysates have been studied to gain an understanding of the mechanism of histamine release in this system. Dinitrophenol produced 80% inhibition of histamine release at a concentration of 10(-3) M. Iodoacetic acid inhibited release to a lesser extent, and deoxyglucose had relatively little effect. Colchicine was a potent inhibitor of release and produced 88% inhibition at a 10(-3) M concentration. Puromycin and cycloheximide had essentially no effect on histamine release. Various sugars inhibited release with mannitol and glucose, producing greater than 50% inhibition at 10(-3) M concentrations. Other sugars inhibited histamine release to a lesser degree with the following order of potency: mannitol > glucose > sucrose > galactose > fructose. These studies suggest that intact, metabolically active cells are required for histamine release induced by human leukocyte lysates and that a secretory process is involved. The results also provide information on the possible nature of the histamine-releasing factor(s) in human leukocyte lysates.
The characteristics of histamine release induced by human leukocyte lysates were determined. Intact human leukocytes released histamine during incubation with leukocyte lysates. Maximal release occurred under physiological conditions of temperature and pH, and both Ca(2+) and Mg(2+) were required. The addition of ethylenediaminetetraacetic acid abruptly inhibited release. Complement was not required, and serum actually inhibited release. Histamine release was maximal at lysate concentrations of 0.25 to 1.0 mug of protein per ml, and it was reduced at either higher or lower concentrations. Leukocytes continued to exclude trypan blue and maintained chemotactic activity after histamine release. Leukocytes released histamine independently of cellular protein or enzymes. Histamine release induced by leukocyte lysates was interrupted by subsequent removal of the lysate. The data suggest that this histamine release occurs by a specific, complement-independent, noncytotoxic process which resembles, but is not identical with, antigen-induced histamine release. The system has several unique characteristics which suggest that it is a novel form of inflammatory histamine release. This system should provide a useful in vitro model for studies of cellular processes in human inflammation.
The role of cyclic AMP in histamine release induced by human leukocyte lysates was investigated. Leukocytes were incubated with leukocyte lysates prepared by ultrasonic disruption, and histamine was determined fluorimetrically. Several cyclic AMP-active agents had a marked inhibitory effect on histamine release. Theophylline and isoproterenol produced 50% inhibition at concentrations of less than 10(-5) M. Prostaglandin E(1) and dibutyryl cyclic AMP inhibited release by 50% at 7 x 10(-8) M and 6 x 10(-5) M concentrations, respectively. Histamine, which has recently been shown to increase leukocyte cyclic AMP, had a pronounced inhibitory effect on lysate-induced histamine release, producing 50% inhibition at a concentration of only 2.5 x 10(-12) M.Leukocytes, incubated with leukocyte lysates, were sampled at various times and assayed for free histamine released into the incubation mixture supernates, and for bound histamine associated with the leukocyte buttons after centrifugation. Theophylline, prostaglandin E(1) and dibutyryl cyclic AMP not only blocked histamine release, but also caused a progressive decrease in free histamine when added at any time up to 30 min after initiation of the release reaction. As the free histamine decreased after addition of the inhibitors, there was a corresponding increase in the bound histamine, suggesting that previously released histamine was reabsorbed by the leukocytes after exposure to cyclic AMP-active agents. Continued incubation of leukocytes in their own histamine after completion of the release reaction also resulted in reabsorption of the previously released histamine. Previous studies have indicated that cyclic AMP inhibits leukocyte histamine release. The results of the present studies suggest that cyclic AMP modulates histamine release induced by human leukocyte lysates by stimulating reabsorption of histamine from the extracellular environment. These studies also suggest that previously released extracellular histamine may stimulate its own reabsorption by increasing the intracellular level of cyclic AMP.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The purification and chemical properties of thymosin, obtained from bovine thymus tissue, are described. The biological activity of the thymic hormone has been assessed by a newly developed rosette assay, which permits measurement of thymus-dependent lymphoid cells. Thymosin activity is associated with a physico-chemically homogeneous protein of molecular weight 12,600. The hormonal activity is evident in in vitro incubation assay, after injection into adult thymectomized mice, and in prolonging survival of neonatally thymectomized mice and the reconstitution of their response to a skin allograft.
A comparative study was made of Formalin-inactivated Chikungunya vaccines prepared from the virus propagated in African green monkey kidney monolayers and concentrated chick embryo suspension cultures. The vaccine prepared in the chick embryo suspension cultures was significantly more protective to mice against a live homologous virus challenge and stimulated the production of 4 to 5 times more circulating antibodies than the vaccine prepared with virus grown in African green monkey kidney monolayer cultures.
Explore the source record for details and available documents.