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Biomedical subjects

M Hayami

Publications and source records attributed to M Hayami.

At least 217 records · Page 12Linked to original sources
PubMed1981

Induction and characterization of splenic suppressor cells directed to natural killer cells in Japanese quails.

Intravenous inoculation of chicken amniotic fluid (ChAmF) markedly reduced natural killer (NK) cell activity of spleen cells from Japanese quails. The reduction of NK activity was mediated by non-adherent thymus-dependent lymphoid cells which were resistant to treatment with anti-immunoglobulin serum and sensitive to treatment with anti-thymocyte serum in the presence of complement. The suppressing activity was selectively directed to NK cells, since Rous sarcoma virus-specific cytotoxicity or hemagglutinating antibody production against sheep erythrocytes was not suppressed in ChAmF-treated quails. Spleen cells from normal 1-week-old quails had similar characteristics to those from ChAmF-treated 4-week-old quails, lacking NK activity and exhibiting suppressive effect on NK activity, and were also shown to be thymus-dependent. Biological significance of the presence of NK cells and their suppressor cells is discussed in relation to embryonic development and tumor-surveillance mechanism.

Amniotic Fluid↗
PubMed1980

Detection of natural killer cells in Japanese quails.

Spleen cells of normal quails exhibited cytotoxicity on normal embryo cells as well as on virus- and chemically transformed cells. Spleen cells responsible for the destruction of target cells were shown to be non-adherent lymphoid cells which lack surface immunoglobulin and are resistant to the treatment with anti-thymocyte serum and complement. Spleen cells of quails which were injected with chicken amniotic fluid (ChAmF) showed no cytotoxic activity. Furthermore, the addition of ChAmF-treated spleen cells abolished the cytotoxic activity of untreated spleen cells. These results indicated the presence of a spleen-cell population in normal quails compatible with mammalian natural killer (NK) cells and the induction of suppressor cells directed to the NK cells by administration of ChAmF.

Amniotic Fluid↗
PubMed1979

Growth of measles virus in continuous cell lines derived from the nervous tissues of human and rat.

Growth of two measles virus strains, the TYCSA and CAM, was compared in three continuous cell lines derived from the nervous tissues, human neuroblastoma IMR-32, human glioma 118MGC, and rat glioma C-6. The two human neural cells were shown to support the growth of both measles virus strains as efficiently as in the non-neural Vero cells. Different types of cytopathic effect (CPE) between the two virus strains were noticed in IMR-32 cells; the CAM strain induced strand-forming type CPE and the TYCSA strain giant-cell type CPE. As a difference of growth pattern between IMR-32 and 118MGC cells, virus antigen was demonstrated in both the nucleus and cytoplasm of 118MGC cells whereas virus antigen was present only in the cytoplasm of IMR-32 cells. In contrast to the productive infection in human neural cells, growth of both virus strains was restricted in rat glioma C-6 cells without showing CPE although the prolonged presence of virus antigens was demonstrated by the immunofluorescent technique.

Animals↗
PubMed1979

Lipid composition of Staphylococcus aureus and its derived L-forms.

Two strains of Staphylococcus aureus (Newman and Tazaki) and their derived L-forms were cultured in serum-containing broth and the differences in their lipid compositions were analyzed. Cardiolipin accounted for more than 50% of the total phospholipid phosphorus in L-forms, but for less than 25% in parent bacteria. The cardiolipin content of L-forms was very high through all growth phases, although it increased gradually as growth proceeded. Significant amounts of cholesterol and its esters were present in parent strains and L-forms, all of which incorporated serum cholesterol into the cell membrane. On the other hand, they could be detected in the L-forms but not in the parent strains when they were cultured in serum-free broth. To examine the ability of L-forms to synthesize cholesterol, the cholesterol content of L-forms cultured in serum-free broth was compared with that of the medium. The results indicated that staphylococcal L-forms could synthesize cholesterol and its esters. These differences in lipid composition suggested that modification of membrane lipids may occur as an adaptational change in response to the disappearance of the cell wall.

Cardiolipins↗
PubMed1979

Presence and synthesis of cholesterol in stable staphylococcal L-forms.

The sterol which was present in two strains of a stable staphylococcal L-form was analyzed by gas-liquid chromatography and combined gas-liquid chromatography-mass spectrometry. The retention time of the sterol on gas-liquid chromatography was the same as that of authentic cholesterol. Analysis of the sterol by mass spectrometry showed a molecular ion at an m/e of 386 and the same patterns of major ions above an m/e of 145 as those of authentic cholesterol. As a result, the sterol in staphylococcal L-form was identified as cholesterol. A parent strain and its L-forms were cultured in medium containing [14C]acetate, and the synthesis of cholesterol was examined. In the L-forms, 0.52% of the total lipid radioactivity was found in cholesterol fraction, whereas no significant radioactivity was detected in the cholesterol fraction of the parent strain, indicating that staphylococcal L-forms have acquired the capacity to synthesize cholesterol.

Cholesterol↗
PubMed1979

Continuous lines of RSV-transformed embryo cells and peritoneal macrophages of Japanese quails.

Four continuous lines of RSV-transformed quail cells were established; QERC-31F and QERC-31N cells derived from quail embryo cells and PERP and PERY cells from adult quail peritoneal macrophages. Marked morphological difference was noted between QERC-31F and QERC-31N; the former showed fusiform shape and the latter nodular shape. Both PERP and PERY showed macrophage-like morphology with phagocytic capacity. All four cell lines contained gs antigen and gp 85. Production of transforming virus was found in QERC-31N, PERP and PERY. In spite of failure in production of transforming virus, EQRC-31F was demonstrated to produce C-type particles by electron microscopy and to contain tumor-specific surface antigen by in vivo immunization and in vitro microcytotoxicity tests.

Animals↗
PubMed1979

Influence of different routes of anti-tumor immunization: alternative induction of tumor immunity and tumor enhancement.

Chickens and quails were immunized in parallel either i.v. or intramuscularly (i.m.) with lectin column-purified antigens from chick embryo cells that were transformed in vitro by avain sarcoma virus (ASV). After five to six injections, immunity of the animals was tested by challenge with ASV into the wing webs. Whereas tumor growth was inhibited after i.v. immunization with respect to incidence rate and time of tumor appearance, tumor growth was enhanced after i.m. injection. Animals that were injected with normal cell antigens served as controls. Spleen cells from only those animals that were immunized i.v. exerted a cytotoxic effect in vitro against ASV-transformed cells, whereas spleen cells from i.m. injected animals, in contrast, suppressed such cytotoxicity. The search for serum blocking or arming factors suggested that sera from i.m. injected animals block cellular cytotoxicity whereas sera from i.v. immunized animals render normal spleen cells cytotoxic (arming effect). The use of viruses from different subgroups and of antigens from gp85-lacking ASV-transformed cells indicates that immune effects were obtained against tumor cell surface antigens that differ from the antigen that is involved in virus neutralization (s-gp85).

Alpharetrovirus↗
PubMed1978

Rous sarcoma virus-transformed avian cells express four different cell surface antigens that are distinguishable by a cell-mediated cytotoxicity-blocking test.

Japanese quails bearing avian sarcoma virus-induced tumors develop immune spleen cells that are cytotoxic in vitro against virally and chemically transformed cells, as well as against embryonic cells. The cell-mediated cytotoxicity can be blocked by soluble antigens extracted from in vitro cultured cells. The existence of partial as well as total blocking effects in tests with extracts from various transformed and untransformed virus-producing cells makes it possible to distinguish up to four different kinds of antigens expressed on sarcoma virus transformed cells: a) a subgroup-specific determinant of the virus-envelope glycoprotein gp85 (s-gp85) is expressed at the surface of productively infected, tranformed as well as untransformed cells; b) a group-specific determinant of gp85 (g-gp85) that is only expressed on the surface of virus-transformed cells; c) embryonic antigens, also detectable on chemically transformed as well as on primary normal embryonic cells, and finally; d) a sarcoma virus transformation-specific antigen (TSSA) that is not a structural constituent of the virus.

Animals↗
PubMed1977

Avian retrovirus-induced surface antigens and their cross-reactivity with chemically-transformed cells and primary embryonic cells of Japanese quails.

By testing spleen cells from avian leukosis (ALV) and avian sarcoma virus (ASV)-injected Japanese quails in a microcytotoxicity assay against various target cells, we have demonstrated the existence of several target antigens. With non-transformed ALV-infected Japanese quail cells used as target cells, an avian retrovirus subgroup-specific destruction was obtained when spleen cells from animals infected with either avaian sarcoma or leukosis virus of the same subgroup were employed. This reaction is probably due to the virus envelope glycoproteins (Ve-gp) expressed on the cell surface. Apart from this subgroup-specific reaction, avian retrovirus group-specific destruction of ASV-transformed cells was demonstrated by means of effector cells immunized with ASV of a different subgroup. This reaction is restricted to transformed cells and not due to the virus envelope glycoprotein because the same effector cells are not cytotoxic to ALV-infected non-transformed cells but cytotoxic to sarcoma-virus-transformed cells which lack Ve-gp. Quail methylcholanthrene-tumor cells which show a transformation phenotype similar to that of ASV-transformed cells but which are free of detectable endogenous and exogenous retrovirus were also destroyed by the spleen cells from ASV tumorbearing animals. The same effector cells also exerted a weak cytotoxic effect on uninfected primary embryo cells but not to embryo cells after several passages.

Alpharetrovirus↗
PubMed1977

Analysis of precursors to the envelope glycoproteins of avian RNA tumor viruses in chicken and quail cells.

Immune precipitation with monospecific antiserum was employed to study the intracellular synthesis of viral glycoproteins gp85 and gp37. Labeled gp85 and gp37 were detected from lysates of cells transformed with Rous sacroma virus, strain B77, after long-term labeling with radioactive glucosamine or phenylalanine. Immune precipitates prepared from lysates of cells pulse-labeled for a short time resulted in a glycoprotein of 92,000 molecular weight (gp92). This precursor was stable in B77-transformed Japanese quail cells for several hours, whereas in chicken cells it could be chased within a few hours into virion glycoproteins gp85 and gp37. Similarly, the precursor for the structural viral proteins, pr76, persisted in quail cells much longer than in chicken cells. During very short pulses or in the presence of a glucosamine block (25 mM glucosamine), the antiserum against the viral envelope glycoproteins detected a precursor of higher electrophoretic mobility of approximately 70,000 molecular weight, "p70." Fucose label entered gp92 and gp85 as well as "p70." Proteolytic treatment of virion-bound gp85 in vitro generated two discrete glycoproteins of 62,000 and 45,000 molecular weight, but did not result in an increase in the amount of gp37.

Animals↗
PubMed1976

Characterization of an early cytotoxicity-inducing factor in sera of Japanese quails after inoculation with Rous sarcoma virus.

By pre-treatment with serum of normal spleen cells used in the microcytotoxicity assay, a humoral factor which induces cytotoxic activity in normal spleen cells was demonstrated in about 40% of sera of Japanese quails as early as 3 days after inoculation with Rous sarcoma virus (RSV). This cytotoxicity-inducing activity was not present either in the IgM or the IgG fraction obtained by Sephadex gel filtration. In sera of quails with experimentally induced agammaglobulinemia, the cytotoxicity-inducing activity was demonstrated at the same frequency as in normal animals. Thus, it seems unlikely that the early cytotoxicity-inducing factor is an immunoglobulin. On the other hand, membrane fractions extracted with 3 M potassium chloride from the RSV-induced quail tumor (QT) cells used as target cells in the microcytotoxicity assay exhibited cytotoxicity-inducing activity. After spontaneous regression of an RSV-induced tumor the serum of the regressor quail contained antibodies specific to the QT cell extract. This serum removed the cytotoxicity-inducing activity of both QT cell extract and serum sampled 3 days after RSV inoculation. In contrast, serum without antibody to the QT cell extract failed to absorb the cytotoxicity-inducing activity of the extract. It is therefore suggested that soluble tumor antigens can act as an early cytotoxicity-inducing factor.

Agammaglobulinemia↗
PubMed1976

Temporal analysis of cellular cytotoxicity and humoral factors during progession and regression of Rous sarcomas in Japanese quails.

Temporal appearance of cellular cytotoxicity and humoral activities including blocking and arming activities during the entire course of Rous sarcoma development in Japanese quails was examined by microcytotoxicity assay with comparison of animals bearing regressing tumors induced by a moderate dose of virus (regressors) and animals bearing growing tumors induced by a large dose of virus (progressors). Cellular cytotoxicity of the spleen cells in regressors was detected in a biphasic pattern; the first phase being observed as early as 3-5 days post inoculation (p.i.), followed by an eclipse period between 7-10 days p.i. which was the time of active tumor growth, and the second phase occurring after 12 days p.i. when the tumor had attained the maximum size. In progressors, only the first phase was observed. Instead, a stimulatory effect of the spleen cells on growth of target cells was noticed. Arming activity which confers cytotoxic activity on the normal spleen cells was demonstrated in the sera of regressors in the similar biphasic pattern as the cellular cytotoxicity; the early activity being present at 3 days p.i., and the late one after 19 days p.i. The former was detected by pre-incubation of serum with effector cells in microcytotoxicity assay and the latter by pre-incubation with target cells. In progressors, only the early arming activity which reacts with effector cells was demonstrated. Blocking activity which abrogates cellular cytotoxicity was demonstrated in both regressors and progressors but in different patterns of appearance, that is, blocking activity in regressors was only transiently demonstrated only by pre-incubation with effector cells at the time of maximum tumor growth, while the activity in progressors seemed to persist after the tumor reached the maximum size. Since the earlier activity was found to be effective at effector cell level, and the later one at both effector and target cell levels, participation of blocking factors of different types in progressors was also suggested.

Animals↗