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N Kono

Publications and source records attributed to N Kono.

At least 235 records · Page 13Linked to original sources
PubMed1982

Pale eosinophilic inclusions simulating ground-glass appearance of cells of hepatocellular carcinoma.

Pale eosinophilic inclusions simulating ground-glass appearance were observed in cells of hepatocellular carcinoma. They were round or elliptical in shape, and their size was about 14 micrometers in diameter. Light eosinophilia and fine granulation with homogeneous appearance were delineated from other cellular materials. They were negative for HBsAg, blood plasma proteins including alpha 1-antitrypsin, and alpha-fetoprotein by immunohistochemical stainings. Ultrastructurally, they were well-demarcated and consisted of homogeneous finely granular matrix. Histological, histochemical and ultrastructural features were different from several intracellular inclusions hitherto reported on hepatocellular carcinoma. These changes may represent a deposition of secretory proteinous materials in cells of hepatocellular carcinoma, but their chemical and antigenetical content could not be identified.

Antigens↗
PubMed1981

An autopsy case of erythropoietic protoporphyria with cholestatic jaundice and hepatic failure, and a review of literature.

A 43-year-old woman with a history of photosensitivity died of hepatic failure following 3 and a half months of unexplained jaundice. The liver was black, showed mild fibrosis and conspicuous pigment deposition in the cytoplasm of the hepatocytes, Kupffer cells and portal macrophages, and within dilated lumina of bile canaliculi and of ductules. The pigment disclosed a striking birefringence and numerous slender electron-dense crystals on electron microscopy. Similar crystals were also found within the cytoplasm of the ductular epithelium. Despite absence of cirrhosis observed in almost all previously described fatal cases the diagnosis of erythropoietic liver with marked protoporphyrin deposition so far have not been described in the cases observed at autopsy.

Adult↗
PubMed1981

Alteration of glycolytic intermediary metabolism in erythrocytes during diabetic ketoacidosis and its recovery phase.

The concentrations of glycolytic intermediates and adenine nucleotides were determined in erythrocytes from patients with diabetic ketoacidosis before and during insulin treatment. Ketoacidosis resulted in an increase in the levels of intermediates above the phosphofructokinase (PFK) step and a marked decrease in the levels of those below this step. Thus, a "crossover" point was seen at the PFK step in a crossover plot. This indicated that the rate of glycolytic flow during ketoacidosis was controlled by PFK and that the reduced level of 2,3-bisphosphoglycerate (2, 3-BPG) was attributed to the inhibition of this enzyme. In vitro studies revealed that acidemia is mainly responsible for the inhibition of PFK, whereas elevated levels of ketone bodies and free fatty acids have no direct bearing on it. Insulin administration produced hypophosphatemia within 8-12 h and it persisted for 24 h or longer. The levels of fructose-6-phosphate and glucose-6-phosphate were decreased transiently during this hypophosphatemic phase, while those of fructose bisphosphate and triose phosphates were increased. This indicated that PFK was activated. Thus, it is no longer reasonable to think that the inhibition of PFK is a factor responsible for a delay in normalization of the 2, 3-BPG level during the recovery phase. The levels of these glycolytic intermediates, including 2, 3-BPG, were normalized within 4 days by appropriate therapy.

Adult↗
PubMed1981

[Autochisel].

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Crowns↗
PubMed1980

Hereditary and acquired abnormalities in erythrocyte phosphofructokinase activity: the close association with altered 2,3-diphosphoglycerate levels.

Specific deficiency of erythrocyte phosphofructokinase (PFK) activity in Type VII glycogenosis presents a good model for the analysis of the relationship between 2,3 diphosphoglycerate (2,3 DPG) level and glycolysis in erythrocytes since glycolytic flow is partially blocked at the regulatory step. Enzymatic analyses of glycolytic intermediates of erythrocytes from a patient with Type VII glycogenosis demonstrated that 2,3 DPG is markedly decreased in parallel with fructose-1,6-phosphate (FDP). In acidosis including diabetic ketoacidosis and uremic acidosis a fall in 2,3 DPG is also associated with a marked reduction in FDP. On the other hand, in respiratory alkalosis glycolytic intermediates shift to the opposite direction and forward crossover at PFK step appears, being associated with an elevation of 2,3 DPG. These data indicate a close relationship between 2,3 DPG level and PFK activity in erythrocytes. At least in acidosis and alkalosis the alteration in 2,3 DPG level may well be explained by changes in PFK activity caused mainly through allosteric mechanism. In addition, twelve cases with hereditary PFK deficiency in muscle and erythrocytes reported in the world are reviewed and discussed briefly.

Alkalosis↗