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Advances in Neurochemistry by Seymour Kaufman (auth.), B. W. Agranoff, M. H. Aprison PDF

By Seymour Kaufman (auth.), B. W. Agranoff, M. H. Aprison (eds.)

ISBN-10: 1461582377

ISBN-13: 9781461582373

ISBN-10: 1461582393

ISBN-13: 9781461582397

In the Preface to quantity 1, we said: This sequence acknowledges that investigators who've entered neurochemistry from the biochemical culture have a slightly really expert view of the mind. Too usually, interdisci­ plinary choices are before everything appealing yet end up to recite uncomplicated biochemical considera­ tions. we've come to think that there at the moment are sufficiently huge numbers of neurochemists to aid a really good enterprise comparable to the current one. we've got all started with attention of conventional parts of neurochemistry which express significant clinical job. we are hoping they are going to serve the neurochemist either for basic interpreting and for specialised info. The reader also will have the ability to mirror at the unbridled hypothesis that effects from the disinhibiting results at the writer who has been invited to put in writing a bankruptcy. We plan sometimes additionally to supply experiences of components now not thoroughly within the area of neurochemistry which we however think to be sufficiently well timed to be known as to the eye of all who use chemical ideas and instruments with a purpose to larger comprehend the mind. The contributions to the current quantity pursue those pursuits. We think the sequence has set excessive criteria and has endured to uphold them. in response to the primary said within the final paragraph of the Preface quantity 1, we contain during this quantity Koshland's "Sensory reaction in micro organism" (Chapter 5).

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5. THE NATURE OF THE GENETIC DEFECT IN CLASSICAL PKU The results of the immunological studies just discussed ruled out only a single possibility for the molecular basis of the phenylalanine hydroxylase deficiency in PKU: normal amounts of a mutant form of the hydroxylase with all its antigenic determinants intact, but devoid of hydroxylase activity, were not present in PKU liver. These results left open the possibility that PKU was caused by a deletion mutation of the gene that codes for the hydroxylase.

PHS deficiency B. Primary defects in another metabolic pathway that indirectly affect the activity of the phenylalanine hydroxylase system. II. , phenylalanine transaminase deficiency. As will be discussed later, there are questions about how realistic this last category is as a possibility. If enzyme assays were available on tissues from all patients with hyperphenylalaninemia, precise diagnosis of the enzyme deficiency would obviously be no problem. The challenge that the field faces today is to try to identify the enzyme deficiency from ~e data that are available.

As it is, there is no way of knowing whether the widely scattered differences in hydroxylase activity that were found were due to differences in phenylalanine hydroxylase levels or to variations in the levels of one of the other ancillary components of the system. An even more serious flaw in methodology probably marred a recent study that claimed to have detected relatively large amounts of phenylalanine hydroxylase activity in liver samples from patients with classical PKU. Using tyrosine formation, determined ftuorometrically, as a measure of phenylalanine hydroxylase activity in liver biopsy samples, Grimm et at.

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Advances in Neurochemistry by Seymour Kaufman (auth.), B. W. Agranoff, M. H. Aprison (eds.)

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