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- W94198205 abstract "In vivo and in vitro studies have shown that the defect in non-ketotic hyperglycinemia (NKH) is due to an abnormality in the glycine cleavage reaction. In the normal human infant, glycine cleavage is shown to occur in liver, kidney, and brain. This chapter discusses the aspect of glycine neurotoxicity in patients with NKH, and in animal experiments, to study the potential of strychnine as an antidote for glycine neurotoxicity. Besides a systematic neurological examination of a newborn infant suffering from NKH, the chapter describes the experiments that aimed to simulate in animals the abnormal glycine concentration found in patients and then to investigate the effect of strychnine administration. The neurological sequence of the patients is in accordance with a glycine neurotoxicity than with a deficiency of some metabolic factor, both because of its sudden onset and because the abnormalities could be simulated in newborn rats by injecting glycine. Moreover, the very rapid change seen in the infant is more likely the result of a toxic action than the expression of an abnormality in a synthetic process. The type of clinical abnormalities shows that the toxicity is expressed as an extreme inhibition of both voluntary and involuntary movements. This is consistent with the idea that the glycine neurotransmission system is hyperactive." @default.
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- W94198205 date "1978-01-01" @default.
- W94198205 modified "2023-09-27" @default.
- W94198205 title "Non-Ketotic Hyperglycinemia (NKH): An Inborn Error of Metabolism Affecting Brain Function Exclusively" @default.
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- W94198205 doi "https://doi.org/10.1016/s0079-6123(08)61024-9" @default.
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