Kenneth A. Hubel
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Kenneth Hubel

Location and chance play a big role in our lives. I graduated from high school in Rye, NY in 1945 in the final days of WWII. I had hoped to enter a naval preflight program but was rejected because of protein in my urine, a sign of possible renal disease. Disappointed, I enlisted in the Navy and was discharged a year later having learned some electronics and having college support from the GI Bill which the pre-flight program would not have granted. I had four years of additional financial support from a competitive NY State veteran's scholarship and a Teagle scholarship available to children of employees of Standard Oil. Dad worked for the company. I graduate from Cornell Medical School in 1954 free of debt and having learned that the urinary protein was benign postural proteinuria..

I was an intern and resident in medicine at Upstate Medical Center in Syracuse. To help support my parents I interrupted residency to work three years at Bristol Laboratories, where I initially oversaw studies of the rates of intestinal absorption of salts of the antibiotic, tetracycline. Some were absorbed better than others for reasons that were unclear. Adrian Hogben at NIH had recently published landmark studies of the effects of lipid solubility and pH on absorption of inert compounds and he had become head of physiology at George Washington University. I asked to join him as a research fellow after I completed 3 years at Bristol and a final year of residency. During that year, I benefited from a course on the biophysics of membrane transport taught by Arthur C. Brown with the strong encouragement of Eugene Jacobson who was then a graduate student in Gordon Moe's physiology department. I married Jan Greer in 1957 and we had 2 girls by the time we moved to Washington in 1960.

Adrian proposed that I study bicarbonate transport in the dog colon; a project that yielded extensive lab experience but no publishable data. In 1962, I was invited to join the faculty of medicine at the University of Iowa where, in the lab, bicarbonate secretion remained my major focus.  Dennis Parsons at Oxford had proposed that bicarbonate was secreted in the mammalian intestine in exchange for chloride. We found that rat ileum in vivo failed to secrete bicarbonate when chloride ions were absent from the luminal solution, thus supporting Parson's hypothesis. My family and I joined Dennis for a memorable sabbatical year in Oxford in 1969 where, in studies with rat small intestine, we found no support for the Ugolev hypothesis that intestinal mucosa enhanced the activity of pancreatic enzymes.

On my return, using cholera toxin to cause high rates of bicarbonate secretion in rabbit ileum in vivo, we demonstrated that bicarbonate accumulated in the lumen because of hydroxyl ion rather than bicarbonate ion secretion. The hydroxyl ions then combined with carbon dioxide to yield bicarbonate. Studies by John Dobbins in the 1980s with vesicles supported this view.

In 1977, in flux chamber studies of rabbit ileum, electrical field stimulation of the intramural nerves caused chloride secretion, an effect blocked by the neurotoxin, tetrodotoxin. The studies provided the first unequivocal evidence that the intrinsic nerves could affect transport of ions by the epithelium. Helen Cooke and her graduate students at Ohio State later extended these studies of the neuropharmacology of secretion using the guinea pig ileum.

I retired in 1998 having had the pleasure of discovering a few new facts of importance and having worked with good people for commendable goals in a stimulating setting where we shared an honorable ethic.


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