Polypeptide mediators of cystic fibrosis. pp. 259-71.

Although complex models involving multiple loci may be plausible, the high frequency 
of cystic fibrosis in Caucasians is probably best explained by selective 
advantage for the heterozygote carrier. In short, an analogy of cystic 
fibrosis with hemoglobin S sickle cell anemia may be greater than 
with Tay-Sachs disease in terms of molecular mechanisms. Protein and polypeptide 
differences have been reported for the humoral fluids of cystic fibrosis 
patients and their heterozygotic relatives in connected with selected bioassay systems. 
These directions relate to a model here proposed for the intermediate 
stages of the physiology of cystic fibrosis, which builds on a 
large body of elegant experimental work. The basic tenet is that 
the cells of cystic fibrosis heterozygotes and normal individuals are in 
a stimulatory loop. Chronic reserpine treatment exaggerates in the normal rat 
a loop similar to the one exaggerated by genetic differences in 
the human, elevating to pathological levels an otherwise normal process. 