Titlebook: Animal Models of Neurological Disease, II; Metabolic Encephalop Alan A. Boulton,Glen B. Baker,Roger F. Butterworth Book 1992 Springer Scien

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Animal Models of Hereditary Hyperammonemias, of the affected individuals, causing an abnormal accumulation of ammonia in the blood. These altered gene products primarily include the enzymes and transport proteins that are part of the Krebs-Hensleit ornithine-urea cycle (.), the principal metabolic pathway for the disposal of ammonia in the ma

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On Causality and Control in Economic Systemsconsiderable study during the past 20 years, and the number of publications related to kindling has increased dramatically (.). Despite efforts to understand kindling and the many parameters that have been explored, the mechanism underlying the phenomenon remains elusive.

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Computing Optimal Tolls in a Money Economyephalomyelopathy (Leigh Disease), as well as in some forms of inherited ataxias. One of the characteristics of a number of these thiamine-deficiency disorders is the predilection to neuropathologic damage of specific regions of the central nervous system (CNS).

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Arnold H. Q. M. Merkies,Marjan W. Hofkesscussed in their respective chapters. In the present chapter, we will discuss several genetic models of epilepsy. These models have unique characteristics that relate to the onset and course of seizure activity.

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Animal Models of the Wernicke-Korsakoff Syndrome,ephalomyelopathy (Leigh Disease), as well as in some forms of inherited ataxias. One of the characteristics of a number of these thiamine-deficiency disorders is the predilection to neuropathologic damage of specific regions of the central nervous system (CNS).

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Animal Models of Hereditary Hyperammonemias,other mutations that hinder the availability of energy-producing substrates necessary for ammonia detoxification at the mitochondrial level have also been included among the list of secondary hyperammonias.