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JAMA. 1963;186(10):946-947. doi:10.1001/jama.1963.03710100084019.
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Classic hemophilia (factor VIII deficiency) and other genetically determined hemorrhagic disorders continue to attract attention, not only because of their dramatic clinical expression but because of the light which the study of these disorders sheds on our understanding of the transmission of inherited diseases. Clinical studies of families afflicted with factor VIII deficiency gave early evidence that the disease was transmitted by a recessive gene located on the x chromosome. With the recognition of canine hemophilia as the clinical and laboratory counterpart of factor VIII deficiency in man, one had an experimental model for testing the genetic hypotheses suggested by the human family studies. By controlled breeding of dogs with canine hemophilia, Brinkhous and his collaborators at Chapel Hill1 firmly established the sex-linked recessive character of the gene responsible for this dyscrasia.

As studies of hemophilia in man have accumulated, it has become apparent that the simple explanation of


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