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Biomedical subjects

W J Cliff

Publications and source records attributed to W J Cliff.

40 records · Page 3Linked to original sources

Dealkylation and loss of capacity for reactivation of cholinesterase inhibited by sarin.

Inhibition of rat brain acetylcholinesterase by (32)P-sarin in vivo results initially in (32)P-isopropylmethylphosphonylated enzyme. The percentage of inhibited enzyme that could not be reactivated by pyridinium aldoxime methochloride (aged enzyme) approximated the amount of radioactivity identified as (32)P-methylphosphonate. The (32)P-isopropyl methylphosphonate not released fromthe inhibited enzyme by the oxime accounted for 51 +/- 10 percent ( standard deviation) of the radioactivity fixed to brain tissue. It showed no correlation with aging and was probably bound to sites other than acetylcholinesterase.

Aging↗

The acute inflammatory reaction in the rabbit ear chamber with particular reference to the phenomenon of leukocytic migration.

Responses to injections of various materials into rabbit ear chambers were studied by in vivo microscopy. The acute inflammatory responses provoked by injections of antibody-antigen complexes were both quantitatively and qualitatively different from the responses obtained after injections of either homologous sera or the antigens alone. The sticking of leukocytes to endothelium during these responses occurred only in the venules draining the injection sites and was frequently present only on the sides of the venules towards the injection sites. An explanation of this finding was proposed in terms of absorption by the minute vessels related to the injection sites of postulated mediator(s) with specific activity on venular endothelium. Analysis of the rates and direction of movement of leukocytes during the reactions produced by the antibody-antigen complexes was performed with the aid of time-lapse cinemicroscopy. The leukocytes that were sticking to the venular endothelium frequently exhibited amoeboid locomotion within the vessels. Twice as many of these cells moved against the direction of blood flow as with it. This finding was discussed and an explanation proposed. A method for detecting a drift in the overall population of emigrated leukocytes within the inflamed tissue was described and revealed that four times as many amoeboid cells moved away from the injection sites as towards them. This result was discussed in the light of the in vitro chemotactic properties of antibody-antigen complexes demonstrated for rabbit leukocytes. An alternative explanation was proposed in terms of variation in the population density of these cells and their random movements and collisions. The rates of amoeboid movement of leukocytes during the acute inflammatory reactions produced by antibody-antigen complexes were similar to the rates found during turpentine inflammation and were compared to other published values.

Animals↗