[Dealing with emergency care. 5. Hemiplegia].
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Biomedical subjects
Publications and source records attributed to T Kanno.
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This is a method for measuring tripeptide aminopeptidase (EC 3.4.11.4) activity in serum. L- Leucylglycylglycine is used as substrate, and the reaction is followed by monitoring the absorbance increase at 340 nm when NAD+ is reduced to NADH in the presence of an excess of leucine dehydrogenase. This principle allows kinetic determination of the enzyme without interference by carboxypeptidases. Amastatin is added to the reaction mixture to prevent nonspecific hydrolysis of the substrate catalyzed by other aminopeptidases. As final reaction concentrations we recommend (per liter): 100 mmol of Tris buffer (pH 8.2), 4.0 mmol of L- leucylglycylglycine , 10 kU of leucine dehydrogenase, 3.8 mmol of NAD+, and 85 mumol of amastatin . The assay is suited to modern enzyme analyzers and has high precision.
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An electrophoretically slow-moving alkaline phosphatase(orthophosphoric-monoester phosphohydrolase, EC 3.1.3.1, alkaline optimum, ALP) isoenzyme was found in the serum of a patient with osteomalacia. Molecular mass of this ALP was estimated to be 500 000 daltons. Inhibitor studies revealed that the abnormal ALP, which formed a macromolecular complex, was an intestinal isoenzyme. Immunofixation following electrophoresis demonstrated that the macromolecular ALP was a complex composed of intestinal ALP and immunoglobulin G of the kappa type. This isotype specificity of immunoglobulin suggested that the ALP immunoglobulin complex is a specific antigen-antibody complex in circulation.
The ultrasonographic appearance of hepatic hemangiomas was studied in 19 patients (31 lesions). The detectability rate by real-time ultrasonography was 77%. A hyperechoic, sharply-marginated and internally homogeneous lesion is highly suggestive of hemangioma. If the hypoechoic lesion has homogeneous internal echoes and/or strong marginal echoes, it is also suggestive of hemangioma. It is difficult to detect small lesions in the lower lateral part of the right lobe and lesions in the right lobe immediately under the diaphragm. Computed tomography should be the next procedure of choice in the evaluation process. If the computed tomography is not characteristic, angiography should be done to confirm the diagnosis.
An amino acid solution enriched in branched chain amino acids (BCAA) was administered to cirrhotic patients with encephalopathy and serial determinations of serum glucose, IRI and IRG were performed. Slight decrease of serum glucose was observed when only BCAA was given. On the other hand, when BCAA was infused with glucose, the serum glucose level decreased significantly after infusion (-77.5 +/- 26.2 mg/dl, p less than 0.01) and two cases of hypoglycemic shock were observed. Although both serum insulin and glucagon increased in these cases, the IRI/IRG molar ratio which was 8.9 at the start of infusion increased to 20.6 at the end of infusion. It was suggested that administration of BCAA with glucose caused hypoglycemia in cirrhotics with encephalopathy, possibly by synergistic action of BCAA and glucose on serum insulin level.
The effects of intracerebroventricular (i.c.v.) injection of synthetic thyrotropin-releasing hormone (TRH) and its analogue (gamma-butyrolactone-gamma-carbonyl-His-Pro-NH2) were tested in anesthetized rats fitted with pancreatic cannula. TRH injection induced dose-related increases in flow of pancreatic juice, protein output, and amylase output, each reaching a maximum within 10 min. Higher doses of TRH induced longer responses. Injection of the TRH analogue also caused dose-related secretory responses of the exocrine pancreas. The dose-related secretory responses to TRH and the TRH analogue were similar except that the responses to the highest dose of TRH analogue (1600 pmol/100 g b.w.) were significantly higher. Intravenous injection of TRH and the TRH analogue induced little, if any, secretory response of the exocrine pancreas. The effects of i.c.v. injection of TRH and the TRH analogue were completely abolished after bilateral subdiaphragmatic vagotomy. In addition to the secretory effects on the exocrine pancreas, i.c.v. injection of TRH and the analogue caused hyperglycemia, tachycardia, and tear secretion, but the intravenous injection of these peptides had no effect.
Surface pressure was found to be produced spontaneously at the interface between air and a suspension containing fragmented sarcoplasmic reticulum (FSR) from rabbit white muscle. Large and stable surface pressure was formed only in a limited concentration range of FSR in the suspension and the pressure formation was proved to be an irreversible phenomenon, suggesting the formation of a monolayer membrane resulting from the disruption of FSR vesicles. Monolayer formation was directly confirmed by analyzing the components included in the membrane and by calculating the surface area occupied by these components. The monolayer included phospholipids, cholesterol and proteins, and appeared to originate from FSR vesicles since the molecular ratios of these components as well as the results of the SDS polyacrylamide gel electrophoresis were similar in both membranes. This phenomenon can be utilized as a method of monolayer preparation from biological membrane vesicles, and should be very useful for the reconstitution of planar biological membranes.
The resorption surface caused by osteoclasts are identified by scanning electron microscopy (SEM), but the morphological interrelation between these resorption surfaces and Howship's lacunae observed by light microscopy remains obscure, and little evidence showing that the distribution and structures of the resorption surface change according to the function of osteoclasts is available. To understand the relationship between the function of osteoclasts and the morphological evidence of bone resorption, surface structures of the parietal bones in mice, newborn to adult, were studied by SEM. The osteoclasts on the inner surface of the calvaria are considered to be involved in the growth of the skull. The outer surface of the parietal bone was smooth, whereas the inner surface consisted of both smooth and rough areas. The rough areas were usually much larger than Howship's lacunae, which are generally thought to be of osteoclast size. These areas were composed of small and shallow concavities with oval or polygonal outlines. The borders between adjacent concavities appeared as ridges. The rough areas were very wide in the growing skull and osteoclasts were scattered on these wide rough areas. The osteoclasts were much larger than the concavities in the rough areas. During the growth of the skull, the proportion of rough areas occupying the inner surface changed parallel to the number of osteoclasts, which varied in correspondence with the growth rate of the skull. The maximum value of the proportion was ab out 60% at 1 week of age. The findings suggest that the osteoclasts resorb the bone by moving along its surface, forming small concavities and leaving rough areas larger than Howship's lacunae of osteoclast size. Furthermore, they suggest that the size and distribution of the rough areas and the morphological features of the concavities in the rough areas vary depending upon the activities of the osteoclasts.
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Different clinical features exist for lactate dehydrogenase A-subunit and B-subunit deficiencies. The metabolic basis for these clinical differences was elucidated by investigating carbohydrate metabolism in the affected tissues. Glycolysis was markedly retarded at the position of glyceraldehyde 3-phosphate dehydrogenase, and significant increases of glyceraldehyde 3-phosphate, dihydroxyacetone phosphate, and fructose 1,6-diphosphate were observed. The physical and kinetic properties of glyceraldehyde 3-phosphate dehydrogenase prepared from human erythrocytes and skeletal muscle were almost identical, but the mode of inhibition of the enzyme was slightly different in erythrocytes and in skeletal muscle. In erythrocytes, impaired reoxidation of NADH followed by the deficiency of substrate NAD+ causes a reduction of glyceraldehyde 3-phosphate dehydrogenase activity. However, in skeletal muscle, the increased level of NADH markedly inhibits the enzyme under anaerobic conditions. A flux of triose phosphates from glycolysis occurred in skeletal muscle of a patient with A-subunit deficiency. This flux is attributable to the high cytosol alpha-glycerophosphate dehydrogenase activity in skeletal muscle. for these reasons the ATP production was significantly impaired in the patient and the damage to muscle cells brings about the release of cytosolic enzymes and muscle rigidity after hard exercise. In contrast in the erythrocytes, the level of alpha-glycerophosphate dehydrogenase is very low and another red cell-specific NADH reoxidizing system such as NADH-cytochrome b5 reductase (NADH-methemoglobin reductase) is operating. In this manner, the NAD+ level in erythrocytes is compensated for without the flux of triose phosphates derived from glucose. Therefore, the ATP production in erythrocytes is sufficiently maintained by glycolysis even in a patient with complete lactate dehydrogenase B-subunit deficiency. Thus, impaired ATP production in anaerobic stage is a condition which is specific for lactate dehydrogenase A-subunit deficiency but does not occur for B-subunit deficiency. The different clinical features of the A- and B-subunit deficiencies have been clearly elucidated.
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