Biomedical subjects
Publications and source records attributed to K Machida.
The mutagenicity of N-nitrosomethamphetamine (NMA) and N-nitrosoephedrine (NEP), which were synthesized in our laboratory, was examined by the modified pre-incubation method of Ames assay using Salmonella typhimurium TA100 and TA98. Both nitroso compounds showed significant mutagenic activity in the presence of hamster S9.
Male and female weanling rats of the SPF Fisher strain were fed purified diets containing three different levels of cadmium (0.008, 0.3, 30 micrograms Cd/g feed). Urine was collected from each animal 1 year after the start of the experiment, and cyclic AMP and cyclic AMP in the urine were measured by radioimmunoassay. Urinary excretion of cyclic AMP and GMP changed in proportion to the intake of Cd. The ratio of cyclic AMP: cyclic GMP, which combined the changes of these two cyclic nucleotides, increased with Cd intake, and these relationships were statistically significantly different in males and females.
A case of hypertrophy of the caudate lobe of the liver is reported in which transmission CT scanning strongly suggested the presence of a liver tumor. However, single photon emission CT using Tc-99m phytate showed that there was only caudate lobe enlargement with no evidence of a space-occupying lesion. The usefulness of single photon emission CT in such situations is discussed.
Twelve cases of aldosteronoma were evaluated with CT and radioisotope scintigraphy to compare the diagnostic capability of both methods. All cases were diagnosed with scintigraphy, while six of 12 cases were diagnosed with CT. However, considering that nuclear imaging requires seven or eight days for evaluation, and the radiation dose is relatively high, it seems reasonable to perform CT scans initially in the localization of an aldosteronoma and to include scintigraphy in those cases in which aldosteronoma is not demonstrated by CT.
Forty-one patients with small cell carcinoma of the lung were treated with a four-drug combination of cyclophosphamide, vincristine, methotrexate, and procarbazine. The response rate was 68% (28 responded among 41 patients), with 10 complete responses (24%) and 18 partial responses (44%). The median survival time from the initiation of chemotherapy was 11 months for patients with limited disease and 8 months for those with extensive disease. Patients who achieved complete response survived significantly longer than those who did not; the median survival time for complete responders was 14.5 months, compared to 8.5 months for partial responders and 6 months for non-responders. Myelosuppressive toxicity remained within acceptable limits, with 5% incidence of leukocytopenia (less than 1,000/microliter) and 7% incidence of thrombocytopenia (less than 50,000/microliter) following the first course of the regimen.
Two new human myeloid cell lines, PL-21 and KCL-22, were established from acute promyelocytic leukemia and chronic myelocytic leukemia, respectively. PL-21 was positive to peroxidase staining and differentiated into mature myeloid cells in vitro. KCL-22 had Ph1 chromosomes and differentiated into granulocytes in vivo.
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Liver scintigrams of 406 cases were interpreted by 11 physicians. The ratios of the interpretation of the physiologically decreased activity areas in the liver scintigrams were 27% in the regions of the porta hepatis, 23% in the gall bladder fossa, 20% in the inferior vena cava, 7% in the renal impression, 2% in the portal vein, 2% in the rib impression and 2% in others. The cases having space occupying lesions showed decreased ratio of the interpretation of the physiologically decreased activity areas, as compared with other groups. Cases of the liver cirrhosis showed decreased ratio in the region of inferior vena cava. Cases using Anger camera demonstrated more increased ratio than cases using a scanner. The 11 physicians could be divided for two groups. One group showed high ratios of the interpretation of the physiologically decreased activity areas, and another group showed very low ratio, because of the different interpretation about the physiologically decreased activity areas in the two groups. In our cases, a very few cases showing decreased activity on the liver image were false positive or false negative for diagnosis of space occupying lesions.
Cardiovascular actions of guanabenz, a new antihypertensive agent, were studied in comparison with those of clonidine and guanethidine. Guanabenz, administered intravenously, produced a rise of blood pressure which was followed by a prolonged fall in anesthetized dogs. Guanabenz also decreased the heart rate, inhibited the respiration, and produced an alteration in T wave and a prolongation of PQ or TP interval in the ECG of the dog. Such effects of guanabenz on blood pressure and heart rate were observed in the cat, rabbit and rat, but there was a slight species-difference in the effects. Clonidine, but not guanethidine, produced responses similar to those of guanabenz. The potency of guanabenz to produce hypotension and bradycardia was approximately 1/10 that of clonidine and 10 times higher than that of guanethidine. The depressor effect of guanabenz was not observed in the spinal cats; thus, the blood pressure rose after the administration. When guanabenz was administered intracerebroventricularly or into the nucleus tractus solitarius of rats, the initial pressor response was not produced, and the depressor and bradycardiac responses were observed. Guanabenz, administered intravenously or intra-arterially, produced an inhibition of cardiac functions, decreased the blood flow of common carotid and femoral arteries, and elevated the perfusion-pressure of the hindlimb in the dog. In the isolated rabbit and guinea-pig atria, guanabenz produced negative inotropic and chronotropic effects and attenuated the rate of rise of the action potential. The contractile responses to serotonin and histamine in the isolated rabbit thoracic aorta were noncompetitively inhibited by guanabenz. From these results, it is suggested that the hypotensive and bradycardiac actions of guanabenz are mediated via central actions, as well as those of clonidine. Furthermore, in addition to the central actions, it was found that guanabenz acts directly on cardiovascular tissues and attenuates the responsiveness.
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