Biomedical subjects
Publications and source records attributed to K Isoda.
A 53-year-old man was found to have a mediastinal mass. Chest X-ray, CT scan, bronchofiber and superior vena vasography showed a left upper giant mediastinal tumor with invasion to left upper lobe and pericardium. And it was performed a surgical treatment and diagnosed a thymic carcinoma (sarcomatoid type) by histological examination. We reported a rare type of thymic carcinoma and added discussion.
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By the microautoradiographic method using 3H-proline, collagen production by mesothelial cells was investigated in adriamycin-induced pleuritis in rats. In subpleural granulation tissue formed at 4 to 7 days after the intrapleural injection of adriamycin, proliferating fibroblasts and primitive mesenchymal cells were most intensely labeled, and abundant deposition of collagen and acid mucopolysaccharides were demonstrated about these cells. It is thus concluded that these subpleural mesenchymal cells are mainly responsible for the fibrosing process. Labeling was also observed in some reactive mesothelial cells and macrophages free-floating in the pleural exudate. Several ultrastructural differences between labeled mesothelial cells floating in the fluid and lining the pleural surface were confirmed, suggesting a change in ability to synthesize collagen during mesothelial desquamation. It seems likely that these labeled mononuclear cells in the effusion, attached to the pleural wound surface, support fibrosis performed by underlying collagen-synthesizing mesenchymal cells. Pleural fibrosis disappeared by 10 days, when mesothelial regeneration was almost complete. Probably this change may be due to fibrinolytic activity caused by regenerative mesothelial cells derived from subpleural mesenchymal cells.
Heat-shock proteins (hsps) are constitutively induced by the mutant actins in the Drosophila indirect flight muscles (IFM). We compared primary structures of the mutant actin genes (KM75 and HH5) which induce hsps and of the non-inducing alleles (KM129 and KM88). The KM75 actin has lost 20 amino acids at the C-terminus. The HH5 actin has only one amino acid substitution, from Gly-336 to Ser. In KM129, the C-terminal part of actin is replaced by novel amino acids. KM88 is a null allele, with an amber mutation early in the coding region of the mutated actin gene. Although all of the KM75, HH5 and KM129 actins have defects near the C-terminus, only hsp-inducing mutant actins cause enlargement of the IFM nuclei as well as a disruption of myofibrils even in the presence of two copies of the normal genes. We further consider the underlying mechanisms linking these features of the hsp-inducing alleles.
Cytologic examination of 3H-thymidine-labeled mesothelial cells in the pleural fluid revealed that single and small-sized cells with slight basophilic cytoplasm scarcely stainable by PAS and colloidal iron are in the DNA-synthetic phase and that these are exfoliating cells from the pleural surface. While abnormal labeling in a few arranged and binuclear cells suggesting accelerated or disturbed mesothelial mobilization was frequently found in congestive cardiac failure, liver cirrhosis, and uremia, it never occurred in single and large-sized activated cells possessing rich PAS-positive granules, cells in large clusters or sheet-like arrangements, or multinuclear giant cells. Transmission electron microscopical observation of these labeled cells proved that a smooth cellular surface and scant intracytoplasmic organelles, by which undifferentiated cells are generally characterized, are essential for DNA-synthesizing mesothelial cells. Probably as a result of some pleural irritation, surface lining cells immediately enter the cell cycle and at once revert to an undifferentiated form capable of DNA synthesis, after which they may be released as a single form, and differentiate and transform into mature, activated cells with a bleb-like surface structure or microvilli, and finally may proliferate in the fluid.
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The incidence of atherosclerosis in hemodialysis (HD) patients is very high. Major risk factors are aging, lipid metabolism disturbances, high blood pressure, and smoking. High blood pressure and hypertriglyceridemia, which is atherogenic in the presence of smoking, are encountered very often in HD patients. The effects of eicosapentaenoic acid (EPA) on plasma lipids and blood pressure were studied for the first time in HD patients by the administration of capsules containing fish oil rich in EPA, which is known to lower serum lipid concentration and blood pressure. We treated 12 hyperlipidemic patients (3 of type IIa, 3 of type IIb, and 6 of type IV; 3 males, 9 females; 31 to 70 years of age; 4 to 90 months on HD) with 24 capsules (1.6 g EPA and 1.0 g docosahexaenoic acid) per day for 13 weeks. Serum triglycerides, total cholesterol, and phospholipid decreased significantly after capsule administration. The ratio of EPA to arachidonic acid in serum increased significantly. There was a small but statistically significant decrease in platelet count. Diastolic blood pressure decreased at the end of the experiment. These effects of fish oil are considered favorable for the prevention of atherosclerosis and its subsequent diseases.
On 34 samples of pleural fluid a cell kinetic study of mesothelial cells was carried out by Feulgen-DNA cytophotometry and the autoradiographic estimation of 3H-thymidine uptake. The generation time of mesothelial cells in malignant effusions was found to be shorter than in non-malignant ones, thought he cellular activity for both effusions was essentially the same. Furthermore, with the development of complicating pleuritis from the early stage to the fibrino-fibrous stage, the appearance rate of 3H-thymidine labeled and activated mesothelial cells in the DNA synthetic phase changed quite differently in both effusions. The differences were thought to be due to neoplastic invasion itself or inflammatory reactions to the neoplastic growth.
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The Feulgen-DNA content of the mesothelial cells in non-malignant pleural fluids was cytophotometrically examined on 21 autopsy cases, in 13 of which (62%) polyploid mesothelial cells with greater than tetraploid nuclear DNA content were found. In 7 the polyploid cells appeared at the rate of 6 to 14%, 6 of which had suffered from uremia or congestive cardiac failure. The appearance rate was closely related to such pleural pathologic changes as prominent edema, diffuse hemorrhage, and fibrin precipitation. The occurrence of these polyploid cells was considered to be the result of mitotic abnormalities in the affected pleural area. Since polyploid mesothelial cells are not rare in certain non-malignant pleural fluids, a trial to establish the diagnosis of malignancy based on DNA cytophotometry alone is not recommended.
Nuclear DNA cytophotometry of the tumor cells was performed for an autopsy case of malignant diffuse pleural mesothelioma diagnosed histologically as a mixed type. The DNA distribution of these tumor cells confirmed bimodality, one being situated in the triploid and the other in the pentaploid DNA range, thus indicating two stemline cell populations. In the former, the majority were epithelial mesothelioma cells resembling the normal mesothelial cells. The latter were mesenchymal tumor cells with spindle and occasionally bizarre shaped nuclei. This cytophotometric data strongly suggests that the histologic variability in mesotheliomas results probably from the change in number and ploidy level of the stemline cell population accompanied by neoplastic development.
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The lactate concentration in antecubital venous blood was determined in 33 patients before and after ischemic forearm exercise. Before exercise, there wa no significant difference in serum lactate level between uremic patients and controls. However, after ischemic exercise the means serum lactate level in uremic patients was significantly lower than that of controls. The results may lead to the conclusion that uremic patients have a markedly reduced ability to form lactate with anaerobic exercise probably due to inhibition of glycolytic enzymes of skeletal muscle.
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