[A case of acute lymphoblastic leukemia with pleural and pericardial effusions as initial and later manifestations (author's transl)].
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Biomedical subjects
Publications and source records attributed to R Abe.
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Retropertioneal tumor is demonstrated by lymphangiography in a 28 year old woman with lymphedema of both legs. Retroperitioneal tumor was subtotally extirpated, with subsequent subsidence of the swelling of both legs. According to the pathologic examination of the extirpated specimens, lymphangiomyomatosis was confirmed. This is the fisrt case reported in the literature of lymphangiomatosis presenting with lymphedema of the leg in the absence of pulmonary involvement, pleural or abdominal effusion.
Lipid metabolic studies were carried out on the male Wistar rats fed on glycerol-rich diet in order to elucidate the mechanism of glycerol-induced hypertriglyceridemia. No difference was found between the glycerol fed rats and the control rats in the rate of triglyceride secretion from the liver measured by the Triton WR-1339 method as well as in the rate of incorporation of labeled glycerol into liver triglyceride. The facts that the half-life of the intravenously injected Intralipid in the blood was significantly delayed in the glycerol fed rats and that the lipoprotein lipase activity released from epididymal adipose tissue of the glycerol fed rats was markedly decreased to 19% of that of the control rats seem to account for the serum triglyceride elevation induced by the glycerol feeding.
The present study was carried out to procure detailed information on the relationship between chronic sodium restriction and renin content of kidneys at a subcellular level in the rat. Renin granules (RG) were separated by a discontinuous sucrose-density gradient (from 1.2 to 1.7 M) centrifugation. In control rats, RG were mainly recovered in the fractions corresponding to 1.5 M sucrose, whereas most of the mitochondria, lysosomes, and microsomes equilibrated in upper fractions. The RG fraction contained approximately 60% of total granular renin activity. Low sodium intake for 4 wk resulted in a 12.4-fold increase in plasma renin activity and led to a 2.6-fold increase in renin activity of the RG fraction. But in sodium-restricted rats there was no alteration in the distribution pattern of renin activity on sucrose-density gradients, indicating that there was no change in the density of RG. These results provide evidence for increased renin activity in storage granules following chronic sodium restriction.
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Smooth muscle cells growing in the primary culture derived from outgrowths of the intimal-medial explants of both rat and human arteries were used. The 72-hr sequential glucose uptake by the cells of both species in culture dishes was enhanced only slightly with time by the addition of insulin to culture medium, and this enhancement was statistically not significant. The glucose conversions to CO2 and lipids by the rat and human cells dissociated for tracer study were not affected significantly during the 2-hr incubation by the insulin addition in vitro. The smooth muscle cells of both species cultured for a week in medium enriched with insulin and then dissociated revealed the significantly increased glucose conversion to lipids, while the increase in the glucose coversion to CO2 was not significant in these cells. Thus, the smooth muscle cells of both rat and human seem to show significant metabolic response to chronic, but not acute, exposure to insulin. Therefore, it is likely that the persistent change in the insulin level may lead to abnormal metabolic state in the artery.
Fifty relatives of 7 families with high prevalence of obesity were investigated and the possibility was shown that there were three forms of familial obesity--normoinsulinemic obesity, hyperinsulinemic obesity and diabetic obesity. In normoinsulinemic obesity, both glucose tolerance and plasma lipids were normal with a few exceptions whereas in hyperinsulinemic obesity, mild glucose intolerance and manifest hyperlipidemia, and in diabetic obesity, blunted insulinogenic index and more advanced glucose intolerance with slight hyperlipidemia existed.
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A lymphatico-osseous communication was demonstrated by lymphangiography in a patient with primary lymphedema of the left leg. The superficial lymph vessels were markedly hyperplastic and contrast medium was visible within the epiphyseal portions of the femur, tibia, fibula, and foot bones. Biopsy of the affected femur showed no abnormality.
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Plasma lipids and lipoproteins, glucose tolerance, plasma insulin response to glucose load, and liver function were examined in 81 relatives of 12 index cases with primary endogenous hypertriglyceridemia, hyperinsulinemia, and hepatic steatosis, as well as in 90 nonrelatives, including the spouses, as controls. Insulin hypersecretion (with or without glucose intolerance), endogenous hypertriglyceridemia, and abnormal liver function suggesting hepatic steatosis were shown to exist in the relatives mostly in combined fashion. Correlation analysis and stepwise multiple regression analysis revealed that the combined disorder developed on the basis of obesity. The incidence of diabetes mellitus was significantly high in the relatives (14.8 per cent) as compared with the normal Japanese population (3.5 per cent). Although the vertical transmission of the combined disorder was noted in almost all pedigrees, the frequency distribution analysis of insulin response, glucose tolerance, and plasma triglyceride showed the histograms of these variables similarly skewed to the right as compared with those of the controls, with no apparent bimodality. In view of the hitherto suggested role of insulin in triglyceride metabolism, it is concluded that hyperinsulinemia coupled with obesity seems to be the basic trait of this form of familial hypertriglyceridemia and hepatic steatosis, though the mode of transmission remains to be elucidated.
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