Page31

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Title Exploring human heredity
Subject Heredity, Human; Medical genetics; Adaptation (Biology)
Description Twentieth Annual Frederick William Reynolds Lecture.
Creator Stephens, Fayette Ellsworth, 1890-
Publisher Extension Division, University of Utah
Date 1956-01-16
Date Digital 2008-05-29
Type Text
Format image/jpeg
Digitization Specifications Original scanned on Epson Expression 10000XL flatbed scanner and saved as 400 ppi uncompressed tiff. Display images generated in PhotoshopCS and uploaded into CONTENTdm Aquisition Station.
Resource Identifier http://content.lib.utah.edu/u?/reynolds,362
Source LD5526 .U8 n.s. v.47 no.11
Language eng
Relation Digital reproduction of "Exploring human heredity" J. Willard Marriott Library Special Collections
Rights Digital Image Copyright University of Utah
Metadata Cataloger Seungkeol Choe; Ken Rockwell
ARK ark:/87278/s64q7rxv
Setname uu_fwrl
Date Created 2008-07-29
Date Modified 2008-07-31
ID 319670
Reference URL https://collections.lib.utah.edu/ark:/87278/s64q7rxv

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Title Page31
Description EXPLORING HUMAN HEREDITY 31 but also because mental traits are difficult to identify, define, and classify. In many cases environment plays an important role in their production, and it is not always possible to evaluate properly the part it plays and the part which is played by heredity. These difficulties are not so evident in the study of some forms of mental deficiency as they are in the study of other mental traits. To speak of the inheritance of mental deficiency is like speaking of hereditary blindness. There are many different kinds, not all of which may be inherited in the same way. In fact some cases may be due to birth injuries or other environmental conditions and have no hereditary basis. The inheritance of phenylketonuria is an interesting example of how a recessive gene may produce one form of mental deficiency. Phenylalanine is an essential amino acid in the body. Several chemical steps are necessary to break it down to the final products, carbon dioxide and water. This seems to be accomplished by a different enzyme at each step. Thus one enzyme is thought to break phenylalanine down to phenylpyruvic acid, and another to break phenyl-pyruvic acid down to parahydroxy phenylpyruvic acid, etc. A recessive mutation in the gene which produces the latter enzyme has taken place so that in some individuals the normal gene does not appear and the phenylpyruvic acid accumulates in the tissues and is excreted in the urine. It can be identified by a simple test which turns the urine dark. In these cases the brain is also affected, resulting in mental impairment ranging from an I.Q. of 90 to practically 0. Here we have a trait which is inherited as a recessive, and the gens which produces it does so because it is unable to produce an enzyme which is necessary to carry on the normal metabolic process. Dr. Marvin D. Armstrong of the biochemical division and Dr. Frank H. Tyler of the clinical division of the University's Laboratory for the Study of Metabolic Disorders have recently reported some very interesting things in connection with this disease. Children with phenylketonuria were given synthetic diets deficient in phenylalanine for varying lengths of time. This treatment was based on the theory that some substance existed in the patient that was detrimental to the central nervous system. Definite improvement in the patients gave evidence of the correctness of this theory. Here we may have an example of a case where knowledge of what
Format image/jpeg
Identifier 031-RNLT-StephensF_Page31.jpg
Source Original Manuscript:Exploring human heredity by Fayette E. Stephens.
Setname uu_fwrl
Date Created 2008-07-29
Date Modified 2008-07-29
ID 319665
Reference URL https://collections.lib.utah.edu/ark:/87278/s64q7rxv/319665