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Titlebook: Cirrhosis, Hyperammonemia, and Hepatic Encephalopathy; Santiago Grisolía,Vicente Felipo Book 1993 The Editor(s) (if applicable) and The Au

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Allgemeine Hinweise zur Reha-Indikationtist and teacher Dr. Santiago Grisolia. The topic of the course, dealing with the relationships of excess ammonia, liver pathology, and brain deficiency, indicates the interrelationships of the various organs in the body, and also indicates the need for us to identify the processes that are unique t
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https://doi.org/10.1007/978-3-030-66352-0e nervous systems (1–3) The activity of these excitatory systems is intimately involved in the processing of incoming information into the spinal cord and brain, the initiation of learning processes, and the formation of memory (2–4). Glutamate neurotransmission involves most brain regions and subse
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Rehabilitation After Limb Salvage Surgeryons and the receiving part of the postsynaptic neurons: the pre- and postsynaptic components are separated by a space termed a synaptic gap. Nerve impulses reaching the presynaptic terminal release a transmitter which is stored in synaptic vesicles preferentially located in the nerve terminal. The t
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Brain Metabolism in Hepatic Encephalopathy and Hyperammonemia,a result of fulminant hepatic necrosis or over many years in chronic conditions such as alcoholic fatty liver or cirrhosis. When the liver fails, or when blood is shunted around a cirrhotic liver directly from the intestines into the systemic circulation, brain function deteriorates: a disorder know
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Ammonia Metabolism in Mammals: Interorgan Relationships,ate nitrogen by reduction of compounds containing nitrogen at its higher oxidation states to the -3 oxidation state (ammonia) which in turn is incorporated into amino acids in a reaction requiring removal of two electrons (1). Until relatively recently it was thought that in mammals all enzymatic re
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Effects of Hyperammonemia on Neuronal Function: NH4 +, IPSP and Cl--Extrusion,equences of these two effects of hyperammonemia on the function of neurons in mammalians . have been reviewed previously (64,65). In brief, the inactivation of Cl-extrusion shifts the equilibrium potential of the inhibitory postsynaptic potential (IPSP, E.) to the level of the resting membrane poten
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