[Critical leakage at the cuff of a tracheal tube used in pulmonary lavage].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to A Masuda.
Explore the source record for details and available documents.
The transdifferentiation of pigmented epithelial cells in vitro is briefly introduced. Several environmental conditions regulating the process have been demonstrated experimentally. On the basis of these data we have suggested regulatory factors in relation to the mechanisms for the initiation of the transdifferentiation of pigmented epithelial cells, focussing particularly on cell surface functions. Finally, we have presented data which contributes to the establishment of a useful and powerful cell culture system which makes it possible for us to analyse the molecular basis of transdifferentiation.
A fungal metabolite, ML236B (Compactin), isolated from Penicillium citrinum, is a specific inhibitor of 3-hydroxy-3-methylglutaryl (HMG)-coenzyme A reductase (EC 1.1.1.34). Three ML236B-resistant (ML236Br) mutants, MF-1, MF-2, and MF-3, were isolated from V79 after N-methyl-N'-nitro-N-nitrosoguanidine mutagenesis. The fluctuation test showed 2.2 X 10(-6) mutants per cell per generation of a spontaneous mutation frequency of ML236Br clones. These ML236Br clones showed a four- to fivefold-higher resistance to the drug than did their parental V79. Radioactive acetate, but not mevalonate, incorporation into the sterol fraction increased about 10-fold in ML236Br clones in comparison with that in V79. The cellular level of HMG-coenzyme A reductase in three ML236Br mutants was found to be a few-fold higher than that of V79 when cultured in the presence of lipoproteins. The 125I-labeled low-density lipoprotein-binding assay showed binding activity in three ML236Br clones comparable to that of the parental V79 cells. By contrast, an internalization assay of 125I-labeled low-density lipoprotein into the cells showed significantly reduced activity in three ML236Br clones in comparison with V79.
Acute and intense hemorrhage in the anterior lobe of the pituitary was observed in mice treated with hypertonic solutions. The onset of hemorrhage and the spontaneous recovery phase were studied with light and electron microscopes. Ten minutes after ip injection of 9% NaCl, 8% NaHCO3, 3 M glucose or 3 M sucrose at a dose of 0.03 ml/g B. W. there was selective bleeding in the anterior lobe of the pituitary. The maximum extent of hemorrhage was reached 12 h after the injection of hypertonic solution and lasted for approximately 3 days. Ontogenetic study indicated that no pituitary hemorrhage occurred in mice younger than 2 weeks of age. Hypophyseal cleft was found to be not merely a residual lumen but an active site providing for accumulation and digestion of blood cells which flowed out of the bleeding anterior pituitary. By the end of a week, the necrotic tissue in the center of the anterior pituitary was replaced by granulation tissue consisting of fibroblasts, macrophages, capillaries and a stack of excess basal lamina.
The antifungal effect of a polyene antibiotic amphotericin B (AMB) was almost completely abrogated by exogenous addition of 0.1 microgram/ml ergosterol in the medium. The cytocidal effect of AMB on Saccharomyces cerevisiae was synergistically enhanced when cultured for more than 4 hours with squalene, an obligatory intermediate molecule for sterol formation. However, we could not find significant increase in cellular level of ergosterol content in the yeast cells fed with squalene.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
89Sr-treated mice injected with concanavalin A (Con A) 24 h prior to infection with Listeria monocytogenes (LM) could not enhance the clearance of LM from the spleen. Adoptive transfer of normal syngeneic spleen cells together with Con A rendered these animals more resistant. Spleen cells of 89Sr-treated or age-matched control mice were stimulated with con A for 24 h, and supernatant fluids were assessed for macrophage-activating factor (MAF), i.e. the ability to activate resident peritoneal macrophages to kill LM intracellularly in vitro. A defective MAF production by spleen cells was observed in 89Sr-treated, 2 week-old, and athymic nude mice. Also, treatment of spleen cells with anti-Thy-1.2 antiserum plus complement inhibited MAF production. Synergism between spleen cells from 89Sr-treated and nude mice did not occur. The cells required for MAF production were relatively resistant to gamma irradiation. Nylon wool filtration did not modify the ability of spleen cells to make MAF. 89Sr-treated mice possess macrophages responsive to MAF derived from normal spleen cells. The data suggest that the failure of 89Sr-treated mice to develop an anti-LM response observed in thi system could be due to a defective capacity to produce protective humoral factors and/or cells in response to Con A.
Treatment of C3H/St mice with 100 microCi of 89Sr weakened their genetic resistance to murine cytomegalovirus (MCMV) infection. The criteria utilized to detect increased susceptibility were: (i) survival of mice; (ii) numbers of MCMV-infected cells in the spleens and liver; and (iii) serum glutamic pyruvic transaminase levels. The natural killer (NK) cell activity of spleen cells from mice treated with 89Sr is very low. However, the NK activities of spleen cells of both normal and 89Sr-treated mice were greatly augmented 3 days after infection with MCMV. These NK cells lysed a variety of tumor cells and shared several features with conventional NK cells, but were not lysed by anti-Nk-1.2 serum (specific for NK cells) plus complement. Splenic adherent cells did not lyse tumor cells themselves but were necessary for the stimulation of NK cells by MCMV. The paradox of high NK cell function and poor survival in 89Sr-treated mice infected with MCMV was a surprise. We conclude that these augmented NK cells, of themselves, cannot account for the genetic resistance of C3H/St mice to infection with MCMV.
The inhibition of the growth of HeLa cells in culture by 6-mercaptopurine was greatly enhanced in combination with retinol, retinal or retinol acetate, but not in combination with retinoic acid or retinol palmitate. The antitumor effect of retinol palmitate combined with 6-mercaptopurine was examined in BDF1 mice with L1210 leukemia. The blood level of retinol, a strong potentiator of 6-mercaptopurine among vitamin A compounds, was increased in BDF1 mice after retinol palmitate injection. Retinol palmitate was found to enhance the antitumor effect of 6-mercaptopurine against murine L1210 leukemia to a significant extent (69% increase in life span).
Explore the source record for details and available documents.
The biochemical and biophysical roles of extracellular calcium ions in HVJ (Sendai virus)-induced cell fusion were studied. (1) Various kinds of cell, such as Ehrlich ascites tumor cells, mouse melanoma cells (B16-CW1 cells) and human epidermoid carcinoma cells (KB cells), could fuse in Ca2+-free medium containing a cheletor, glycoletherdiaminetetraacetic acid, in the same way as in Ca2+-containing medium. (2) The ATP content in Ehrlich ascites tumor cells decreased rapidly when the cells were treated with the virus in Ca2+-free medium but not in Ca2+-containing medium. (3) Intracellular adenine nucleotides leaked out into the reaction medium when the cells were treated with the virus in Ca2+-free medium but not in Ca2+-containing medium. (4) On addition of the virus, O2 consumption of Ehrlich ascites tumor cells decreased in Ca2+-free medium, but not in Ca2+-containing medium. (5) HVJ (Sendai virus) did not affect production of lactate by Ehrlich ascites tumor cells in both Ca2+-free medium and Ca2+-containing medium. These observations suggest that the role of extracellular Ca2+ in virus-induced cell fusion is to maintain the ATP and other intracellular metabolite contents at normal levels instead of triggering the fusion reaction itself.
Explore the source record for details and available documents.
A case of extradural nasal and orbital extension of a glioblastoma multiforme in the absence of previous surgical intervention is presented. Such penetration by a glioma is rare due to the natural resistance of the dura mater.
Explore the source record for details and available documents.
The activities of monocytes from lepromatous (LL) and tuberculoid (TT) leprosy patients were studied in a variety of in vitro systems. In assays of receptor activity, increased densities of Fc and C3b receptor sites were observed in monocytes of LL and TT patients as compared to normals. No differences were observed between the polar forms of the disease. Similar results were obtained in the nitroblue tetrazolium (NBT) reduction test. Glucosamine incorporation by monocytes from LL and TT patients was not significantly different from that by monocytes from normal controls. A diminished monocyte spontaneous migration and chemotactic activity to lymphocyte derived chemotactic factor (LDCF) was found in both forms of the disease. Plasma inhibitory factor of monocyte chemotaxis was more evident in the lepromatous form of the disease.
Explore the source record for details and available documents.
Explore the source record for details and available documents.