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G Cave

Publications and source records attributed to G Cave.

5 recordsLinked to original sources
PubMed1998

The effect of chemotaxis and chemokinesis on leukocyte locomotion: a new interpretation of experimental results.

A mathematical model is developed to describe the motion of leukocytes through a Boyden chamber. The model is based on the Keller-Segel model of cell motion and comprises three partial differential equations which describe the evolution of the neutrophils, the chemoattractant, and a neutrophil-derived chemokinetic factor. Where other authors have concentrated on chemotaxis, here attention is focused on the manner in which the chemokinetic factor influences neutrophil locomotion. Numerical simulations show how the number of neutrophils initially placed on top of the chamber affects cellular motion through the system and reproduce the qualitative behaviour observed by Takeuchi & Persellin (Am. J. Physiol. 236, C22-C29). In particular, the simulations show how dense packing of the neutrophils increases the levels of the chemokinetic factor. This enhances random cell motion and increases the speed with which the neutrophils reach the source of chemoattractant. For a particular asymptotic limit of the system parameters, the model reduces to a nonlinear partial differential equation for the neutrophils. Similarity solutions of this caricature model yield algebraic expressions relating the speed with which the neutrophil front penetrates into the chamber to the number of neutrophils initially placed on top of it. The implications of the results are also discussed.

Cell Movement↗
PubMed1989

Heart rate and blood pressure changes during sleep-waking cycles and cataplexy in narcoleptic dogs.

Cataplexy is the abrupt loss of muscle tone experienced by narcoleptics. It is usually precipitated by strong emotions or athletic activity. It has been hypothesized that cardiovascular variables have a role in the triggering of cataplexy. In the present study, we have utilized the narcoleptic canine model to directly investigate changes in heart rate and blood pressure in relation to cataplectic episodes. We found that heart rate increased 18% on average in the 20 s preceding cataplexy onset and then fell during cataplexy. Thus, from a cardiovascular standpoint, cataplexy can be subdivided into two very different periods, the cataplexy onset period with very high and declining heart rate, and the period greater than or equal to 10 s after onset, with greatly reduced heart rate. Heart rate at cataplexy onset was significantly higher than heart rate in rapid-eye-movement (REM) sleep, non-REM sleep, and quiet waking. Blood pressure did not markedly change before the onset of spontaneous cataplexies but decreased significantly during cataplexy. Although blood pressure increases did not precede spontaneous cataplexies, sudden increases in blood pressure, induced pharmacologically or by obstruction of the descending aorta, triggered cataplexy in the most severely affected subjects. A hypothesized role for cataplexy as a homeostatic reflex, triggered by interactions between blood flow, central chemoreceptors, and atonia control mechanisms in the medial medulla, is discussed.

Animals↗