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Oxygen dissociation curves were determined in mammalian blood at the CO2 tension of the organism, without the addition of buffers, dilution of the blood, or other alterations. It appears that the dissociation curve is related to body size in such a way that the blood of smaller animals has a higher unloading tension for oxygen. This finding is discussed in relation to the higher metabolic need for oxygen of the smaller animal. It is suggested that, in addition to the higher capillary density in the small animal, a higher unloading tension for oxygen also contributes to the steepness of the diffusion gradient for oxygen from the capillary to the tissue cells.

The Drosophila slowpoke gene encodes a BK-type calcium-activated potassium channel. Null mutations in slowpoke perturb the signaling properties of neurons and muscles and cause behavioral defects. The animals fly very poorly compared with wild-type strains and, after exposure to a bright but cool light or a heat pulse, exhibit a "sticky-feet" phenotype. Expression of slowpoke arises from five transcriptional promoters that express the gene in neural, muscle, and epithelial tissues. A chromosomal deletion (ash2(18)) has been identified that removes the neuronal promoters but not the muscle-tracheal cell promoter. This deletion complements the flight defect of slowpoke null mutants but not the sticky-feet phenotype. Electrophysiological assays confirm that the ash2(18) chromosome restores normal electrical properties to the flight muscle. This suggests that the flight defect arises from a lack of slowpoke expression in muscle, whereas the sticky-feet phenotype arises from a lack of expression in nervous tissue.

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