[Composition of parenteral amino acid solutions prepared for hepatic failure: theories and clinical studies].
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Biomedical subjects
Publications and source records attributed to T Okada.
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A study of 52 liver biopsies (47 hepatitis type B and 5 asymptomatic carriers) was performed to clarify the roles of HBe antigen (HBeAg), HB surface antigen (HBsAg) and HB core antigen (HBcAg). In this study, the Gudat classification was modified so as to classify the patterns of HB antigens into six reaction types including: type O (negative for both liver HBsAg and liver HBcAg), type III-A (characterized by a spotty HBsAg pattern) and type III-B (characterized from a sub-lobular to lobular HBsAg localization pattern). This classification enabled accurate prediction of the prognosis of hepatitis. Patients with positive serum HBeAg had either minimal hepatitis with mild clinical features or chronic aggressive hepatitis with severe clinical features. Ten patients negative for both HBeAg and HBeAb were all positive for liver HBcAg. In all 3 patients on corticosteroid administrations liver tissue was markedly positive for HBcAg and serum was usually positive for HBeAb.
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Benzodiazepines bind with high affinity to a specific benzodiazepine receptor, which occurs exclusively in the central nervous system. The affinity of various benzodiazepines to the receptor closely parallels their pharmacological and therapeutic potency. Binding to the receptor is stereospecific. The receptor is mainly localized in the synaptic membrane fraction and has its highest density in cortical areas of the brain. In Huntington's chorea a decrease in benzodiazepine receptor binding is found in caudate nucleus and putamen, which, at least in putamen, is due to a loss of benzodiazepine receptors apparently located on GABA neurones, which degenerate in Huntington's chorea. The loss of benzodiazepine receptors might explain why the ameliorative effects of benzodiazepines in the early stages of the disease are not sustained in the later stages.
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