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Biomedical subjects

M Maeda

Publications and source records attributed to M Maeda.

At least 1,423 records · Page 79Linked to original sources

Murine lymphoma L5178Y cells resistant to purine antagonists: differences in cross-resistance to thioguanine-platinum(II) and selenoguanine-platinum(II).

To determine whether the antitumor activities of thioguanine-platinum(II) [TG-Pt(II)] and selenoguanine-platinum(II) [SeG-Pt(II)] are due to direct actions of these compounds or to the actions of their hydrolysis products, studies were made on a purine antagonist-resistant, murine lymphoma L5178Y/MP subline that lacked the anabolic enzyme hypoxanthine-guanine phosphoribosyltransferase necessary for tumor inhibition. The L5178Y/MP subline proved to be highly resistant to both TG-Pt(II) and thioguanine; the resistance ratios to the two compounds were almost identical. The subline showed high resistance to selenoguanine, but the cross-resistance to SeG-Pt(II) was negligible. Whether the compounds exhibit the delayed cytotoxicity characteristic of purine antagonists was also investigated. Delayed cytotoxicity was demonstrated for TG-Pt(II) as well as for thioguanine and other purine antagonists but not for SeG-Pt(II) or cis-dichlorodiammineplatinum(II). Experiments on cross-resistance and delayed cytotoxicity showed differences in the cytotoxicities of TG-Pt(II) and SeG-Pt(II): TG-Pt(II) exerted its activity through its hydrolysis product thioguanine, whereas SeG-Pt(II) compound was cytotoxic itself.

Animals↗

Histologic and histochemical investigation of Gaucher cells.

Electron microscopic investigations suggest that morphologically, Gaucher cells and histiocytes are very similar. The fact that there are tubular elements in the lysosomes strongly suggests the possibility of lysosomes as the precursors of Gaucher bodies. By means of the lectin staining methods, the localization of glucocerebroside is clearly demonstrable in Gaucher cells. Lectin staining is the significant diagnostic feature of both Gaucher's and Krabbe's diseases.

Biopsy↗

Hematopathological changes in dead and moribund chicks induced by chicken anemia agent.

Fifty day-old chicks were inoculated wit the Gifu-1 strain of chicken anemia agents. They began to show anemia and a drop in body weight 10 days postinoculation. Thirty-five of them died over a period of 12 to 23 days, mostly between 14 and 18 days postinoculation. Hematocrit value and red and white blood cell counts were markedly reduced in moribund birds. Polychromatic erythrocytes and granulocytes dropped in incidence in the peripheral blood accompanied with a fall in hematocrit value, and gained again with recovery from anemia. Macroscopically, dead and moribund birds revealed yellow bone marrow, marked atrophy of the thymus and bursa of Fabricius, discoloration and swelling of the liver, spleen and kidneys. In some cases, there were partially well-defined necrotic foci in the liver, round heart, fresh hemorrhages in the proventricular mucosa, erosion on the gizzard mucosa, and subcutaneous edema. Microscopically, marked hypoplasia or aplasia of hematopoietic cells in the bone marrow and severe depletion of lymphocytes in lymphoid organs, such as the thymus, bursa of Fabricius, spleen, and cecal tonsils, were commonly seen in affected birds. The changes described above suggested that the anemia induced by chicken anemia agent might closely be related to the bone marrow function.

Anemia↗

[Transfer of fosfomycin into the cerebrospinal fluid].

After the fosfomycin (FOM) infusion, its levels in serum and cerebrospinal fluid (CSF) were repeatedly measured in 8 cases without meningitis. 1. The peak concentration of FOM in CSF was 15.5 micrograms/ml with the average of 10.3 micrograms/ml and was reached at 240 minutes with the average of 210 minutes after the infusion. The biological half life time of FOM in CSF was 2 to 6.5 hours. 2. The peak concentration in CSF was compared with it in serum. The average ratio was 4.3 per cent. Each area under the curve (AUC) of FOM concentration in CSF and serum was calculated and average of their ratio was 9.0 per cent. 3. In a case with middle cerebral artery aneurysm, FOM transferred into CSF with ease. The lowest diffusion into the CSF was shown in 2 cases of meningioma. In 3 cases of hypertensive intracerebral hemorrhage with intraventricular perforation, FOM moderately transferred into CSF.

Adolescent↗

Effect of alpha-glucosidase inhibitor on human pancreatic and salivary alpha-amylase.

The mode of inhibition of a new complex oligosaccharide that inhibits the alpha-glucoside hydrolase activity of pancreatic and salivary alpha-amylase was studied. Kinetic analysis revealed a non-competitive type of inhibition with a Ki of 1.47 +/- 0.03 micrograms when tested against human pancreatic alpha-amylase and 3.89 +/- 0.08 micrograms against human salivary alpha-amylase. The inhibitory action of alpha-glucoside hydrolase inhibitor (alpha-GHI) on pancreatic amylase was observed over a wide range of pH (6.0--7.9), whereas the inhibition of salivary amylase was optimal at pH 6.5. Column chromatographic investigations suggested the possible formation of an enzyme-inhibitor complex because the mixture of alpha-GHI and pancreatic alpha-amylase was eluted as a single component through a Sephadex G200 column. However, this enzyme-inhibitor complex was easily separated into each component and the enzyme activity was fully recovered after electrophoresis.

Amylases↗