Biomedical subjects
Publications and source records attributed to M Morimoto.
A novel antibiotic, prothracarcin was isolated from the culture broth of Streptomyces umbrosus subsp. raffinophilus DO-62. The antibiotic has the molecular formula of C14H14N2O and belongs to the pyrrolo [1,4]benzodiazepine antibiotics. Its structure has been elucidated by mass and NMR spectra. It is active against Gram-positive and Gram-negative bacteria and experimental murine tumor sarcoma 180 and leukemia P388.
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Tissue distribution, excretion and stability of 7-N-(p-hydroxyphenyl)-mitomycin C (M-83) in normal mice were compared with those of mitomycin C (MMC) by microbiological assay. M-83 was more rapidly inactivated by mouse liver homogenate in vitro than MMC. MMC could not be detected by thin-layer chromatography-bioautography in the reaction mixture of M-83 incubated with mouse liver homogenate, or in the mouse urine. Both M-83 and MMC exhibited biphasic serum elimination characteristics after iv bolus injection. When these compounds were administered at their approximate LD50 (M-83, 20 mg/kg; MMC, 8 mg/kg) iv into mice, their half-lives were 17.9 and 19.8 min, respectively. However, the half-life of M-83 (10.2 mg/kg) after iv bolus injection was 7.5 min and was shorter than that of MMC (8 mg/kg) at the molar equivalent dose. In ip administration of an approximate LD50, M-83 and MMC exhibited similar drug absorption and elimination patterns. When both compounds were administered iv at the approximate LD50, the 24-hr urinary recoveries of unchanged M-83 and MMC were 2.85 and 19.26%, respectively. The distribution of M-83 in various tissues was similar to that of MMC.
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The antibacterial activities of Staph. aureus isolated in 1980 and 1981 at all districts in Japan to ABPC, CEZ, CMZ and GM were tested. Numbers of test strains were 587 strains in 1980 and 700 strains in 1981, respectively. The frequencies of ABPC and CEZ resistant strains of Staph. aureus (MIC: greater than or equal to 25 micrograms/ml) were clearly increased in annual variation. The percentage of CEZ resistant strains in 1981 tested by 10(8) CFU/ml inoculum size was 12.3%, but the same of CMZ was only 0.6%.
Growth of the secondary Meth 1 tumors, which had been inoculated s.c. in the abdomens of BALB/c mice bearing primary Meth 1 tumors in the flanks, was inhibited as compared with that of tumors in the normal mice, suggesting the development of concomitant antitumor immunity. When levamisole (LMS, 0.625 or 2.5 mg/kg) was administered i.p. to the Meth 1-bearing mice daily before or after secondary inoculation, growth inhibition of secondary tumors was augmented. This effect of LMS was suggested to be tumor specific as evidenced by no growth inhibition of secondary Meth A tumors in mice bearing primary Meth 1 tumors. The spleen cells of 11-day Meth 1-bearing mice exhibited growth-inhibitory activity against Meth 1 cells in the Winn assay. Administration of LMS augmented the growth-inhibitory activity. This effect of LMS was mediated by nonadherent spleen cells and completely lost by the preincubation with anti-Thy 1.2 antibody and complement. Cytotoxicity was detected in the spleen cells of Meth 1-bearing mice by 51Cr release assay after in vitro sensitization with mitomycin C-treated Meth 1 cells. In vivo administration of LMS augmented the cytotoxicity, which was tumor specific and completely lost by the preincubation of the spleen cells with anti-Thy 1.2 antibody and complement. These results suggest that the growth-inhibitory effect of LMS against secondary tumors was mediated by cytotoxic T-cells.
1) Levamisole(LMS) augmented the ability to inhibit specifically the growth of secondary Meth 1 tumors in Meth 1-bearing BALB/c mice. 2) When spleen cells of Meth 1-bearing mice were restimulated in vitro with MMC-treated Meth 1 cells, cytotoxicity became detected by 51 Cr release assay. Such cytotoxicity was augmented by in vivo treatment with LMS. The cytotoxicity was tumor-specific and completely abrogated by incubation with anti-thy 1.2 antibody and complement before the assay. 3) Cytostatic activity of peritoneal macrophages induced by i. p. inoculation with MMC-treated Meth 1 cells was augmented by LMS treatment of Meth 1-bearing mice but such an activity was not Meth 1-specific. 4) LMS did not augment the natural killer cell activity of the spleen cells of BALB/c mice or BALB/c nude mice. These results suggested that the growth-inhibitory effect of LMS against secondary tumors was mediated by cytotoxic T-cells.
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Malignancy and antigenicity of fibrosarcoma Meth 1 cells induced in a BALB/c mouse were compared with sarcoma Meth A cells. Furthermore, antitumor effect of levamisole (LMS) against Meth 1 cells and its immunological mechanism were studied. 1) The lifespan of BALB/c mice inoculated i.p. with 10(2) Meth 1 cells was prolonged by the treatment with LMS. 2) Growth of s.c. inoculated secondary tumors was tumor-specifically inhibited in solid Meth 1-bearing mice as compared with that in non-tumor-bearing mice. Administration of LMS (0.625 or 2.5 mg/kg) augmented the growth inhibition of these secondary tumors. 3) Spleen cells of Meth 1-bearing mice showed a growth-inhibitory activity against Meth 1 cells in Winn assay. LMS (0.625 or 2.5 mg/kg) augmented such a growth-inhibitory activity of spleen cells. The activity was attributed to non-adherent, thy 1-positive spleen cells.
One hundred and seven patients with ventricular septal defect who survived one and a half to thirteen years after hypothermic open-heart surgery were reviewed with respect to somatic, intellectual, and psychomotor development. There were no negative effects associated with deep hypothermic arrest in any of these areas. Abnormal electroencephalograms were seen in one-half the number of patients examined, but there was no close relation between the circulatory arrest period and electroencephalographic findings. CT scanning of the brain indicated that the abnormality decreased with the lapse of the time after hypothermic open-heart surgery. It would appear that hypothermic open-heart surgery with limited circulatory arrest is a useful method, providing that the circulatory arrest is not allowed to exceed a limited period. However electroencephalographic assessment suggests that postoperative cerebral abnormalities may occur more frequently than previously suspected, despite the lack of preoperative abnormalities on the electroencephalograms.
In order to clarify the inhibitory mechanism of insulin secretion associated with open-heart surgery, the influence of insulin antagonistic hormones on insulin secretion was studied in 20 patients with congenital heart diseases undergoing open-heart surgery, under simple deep hypothermia. Despite a hyperglycemia, plasma immunoreactive insulin and C-peptide showed no change during the cooling period, while with the exception of plasma human growth hormone, dopamine-beta-hydroxylase, immunoreactive glucagon, cortisol and cyclic AMP in plasma, either showed no change, or a decrease during the cooling period. It is assumed that catecholamine, glucocorticoid and glucagon do not play an important role in the inhibitory mechanism of insulin secretion during hypothermic open-heart surgery, and a transient hypofunction of the pancreas as well as the liver and the adrenal gland is probably involved.
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Plasma kallikrein activity and plasma serotonin were studied during and after open-heart surgery in 15 patients with extracorporeal circulation and in 15 patients with surface-induced deep hypothermia. Following results were obtained: 1) Plasma kallikrein activity which reflects the activation of the kinin system, showed no significant change during extracorporeal circulation, and significantly increased three hours after the termination of perfusion. However, there was no significant difference in plasma kallikrein activity between the patients with and without low cardiac output syndrome (LOS). In surface-induced deep hypothermia, plasma kallikrein activity showed no significant change during and after operation. 2) Plasma serotonin significantly decreased during both extracorporeal circulation and hypothermia. Moreover, there was no significant difference in plasma serotonin between the patients with and without postoperative LOS or pulmonary hypertension. It is assumed that plasma serotonin may not play an important role in regulating blood pressure during or after open-heart surgery with either extracorporeal circulation or surface-induced deep hypothermia.