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Biomedical subjects

B B Fuks

Publications and source records attributed to B B Fuks.

At least 37 records · Page 2Linked to original sources
PubMed1986

[Analysis of changes in natural cytostatic and cytotoxic activity of mouse spleen cells after treatment with cyclophosphamide and alpha-interferon].

Cytostatic and cytotoxic activity of mouse spleen cells against normal and tumour target cells has been studied. The comparative analysis of mouse spleen cell cytostatic and cytotoxic activity after exposure to cyclophosphamide has shown that the effectors of natural cytotoxic activity are highly sensitive to cyclophosphamide, while cytostatic effectors are heterogeneous in their sensitivity to cyclophosphamide. Pretreatment of spleen cells with alpha-interferon produced an increase in cytotoxic and cytostatic activity against tumour target cells. The cells of lymphoid organs (spleen, bone marrow, thymus) had greater distinctions in cytotoxic than in cytostatic activity against tumour target cells.

Animals↗
PubMed1986

[Isolation and analysis of monoclonal antibodies against various gangliosides].

Female BALB/c mice were immunized with human melanoma (Mewo) cells containing ganglioside GD3 as a surface antigen. Immune splenocytes were fused with syngeneic P3-X63.Ag 8 myeloma cells. Antibodies produced by hybrid clones were analyzed by solid phase immunoassay. B, C, D and Q clones producing antibodies against Raja clavata brain gangliosides were obtained. Monoclonal B and C antibodies bound monosialogangliosides. Monoclonal D antibody bound a number of gangliosides but reacted predominantly with GD1a. Monoclonal Q antibody reacted selectively with GQ1c. It is assumed that ganglioside GQ1c is expressed on the melanoma cell surface and may be found only in the early stage of ontogenesis of high vertebrates.

Animals↗
PubMed1985

[Study of the molecular and cellular mechanisms of action of lipid immunomodulators].

Within a narrow range of low concentrations (0.03-0.12 microgram/ml) polysialogangliosides containing unsaturated fatty acids in the lipid moiety of the molecule activate in vitro the proliferation of lymphocytes, synthesis of interleukin 2 and generation of highly active natural killers which are capable (in a [51Cr] test) of killing syngeneic, allogenic and xenogeneic tumor cells growing in vitro or maintained in mice (YAC-1, K562, Mch-11, SA-1, P-815, EL-4, Ehrlich carcinoma cells). We have developed biomethodology which allows one to introduce adequate concentrations of potent polysialogangliosides and phospholipids into specific macro- and microcompartments of immune system using two essentially different carriers. In experiments on mice this procedure leads to irreversible regression of subcutaneous nodules of syngeneic leukemias and sarcomas (EL-4, YAC, SA-1, Mchs-11) and of Ehrlich carcinoma with an initial size up to 1 cm, as well as to regression or prolonged inhibition of syngeneic cancers (Lewis and AMS-1) with nodules sizes up to 4-5 mm. Added cyclophosphamide increases this effect.

Adjuvants, Immunologic↗
PubMed1985

[Action of phospholipids and gangliosides on tumor cell sensitivity to the cytostatic and membrane-toxic action of splenic effectors].

The authors attempted to study which parts of the lipid molecules are most responsible for an increase in the sensitivity of the tumor cell to the cytostatic and membrano-toxic action of natural spleen effectors. Use was made of different combinations of egg phosphatidylcholine, phosphatidylethanolamine, cardiolipin, dipalmitoyl phosphatidylcholine and a mixture of bovine brain gangliosides. Introduction of phosphatidylethanolamine into the membrane of tumor cells increased, that of phosphatidylcholine and cardiolipin did not change whereas introduction of a mixture of brain gangliosides reduced their sensitivity to spleen effectors. Introduction of brain gangliosides together with egg phosphatidylcholine into the membrane of the target cell increased whereas that together with dipalmitoyl phosphatidylcholine reduced its sensitivity to spleen effectors. It is concluded that the increase in the sensitivity of the tumor cell primarily depends on changes in the lipid template of its membrane, induced by unsaturated fatty acids of egg phosphatidylcholine, and to a less degree on the properties of carbohydrate heads of gangliosides.

Animals↗
PubMed1985

[Comparative analysis of the action of thymic and cerebral GD3 gangliosides on the sensitivity of tumor cells to natural splenic effectors].

Thymic gangliosides GM3 and GD3 and LacCer incorporated into the membrane of the tumor target cell leukemia (YAC) increase its sensitivity to the membrane toxic action of spleen effectors. Unlike thymic gangliosides GD3, ganglioside GD3 of the brain origin substantially reduces tumor cell sensitivity to spleen effectors. Some other brain glycosphingolipids differing essentially in the structure of the carbohydrate part of the molecule exert the same action. It has been shown in model experiments with incorporation into the tumor cell membrane of brain ganglioside GD3 combined with thymic LacCer or with egg phosphatidylcholine that the increase in the sensitivity of the tumor cell membrane to spleen effectors is linked with a change in the properties of the lipid membrane matrix under the effect of unsaturated fatty acids (e.g. in experiments with phosphatidylcholine). It follows from the data presented that the capability of influencing the sensitivity of tumor cells to natural spleen effectors largely depends on the differences in the structure of the cearamide part of brain and thymic GD3.

Animals↗
PubMed1984

[Effect of interferon and its liposome-incorporated inducer on the recovery of natural killer activity after immobilization stress].

In this work the data on the decrease of the activity of natural killer cells, determined in the test of the release of radioactive chromium from labeled target cells YAC-1 in CBA and BALB/c mice after stress caused by 6-hour immobilization, are presented. The use of mouse leukocyte interferon and the agents inducing its synthesis (double-helical RNA and poly I X poly C, especially poly I X poly C contained in liposomes) has been shown to be highly effective for the restoration of the activity of natural killer cells after its suppression at the period following the stress. The probable role of deficiency of interferon-inducing agents in the mechanisms of decrease of natural cell-mediated cytotoxicity after stress is discussed.

Animals↗
PubMed1983

[Reversible injuries of the natural killer cell membrane after contact with tumor cells].

Injuries to the normal killer membrane were studied during contact with tumor cells on isolated tumor cell-lymphocyte conjugates. The properties of the lymphocyte membrane were shown to undergo changes in the area of contact with the tumor cell membrane, manifesting in the increased membrane permeability for ribonuclease molecules. This effect was more pronounced if lymphocytes were used, in which the synthesis of RNA was suppressed.

Animals↗
PubMed1982

[Ultrastructure and interaction of normal killer cells from human blood and target cells sensitive to them].

Morphological properties of cells possessing a natural cytotoxic activity obtained from blood of healthy persons have been studied, as well as the process of their interaction with sensitive target-cells (K-562). By means of electron microscopy, during incubation at 37 degrees C, appearance of specific morphological manifestations of cytolytic action of the effector-cells forming rather tight contacts with the target-cells (vacuolization of cytoplasm, ring-form defects in plasmalemma, subsequent destruction of the target-cells) has been followed. Morphological features of cytotoxic leucocytes are similar to the morphological criteria specific for T gamma (T-lymphocytes possessing receptors for Fc-fragment of immunoglobulin G) and zero lymphocytes: a rather low nuclear-cytoplasmic ratio, a well developed Golgi complex, a rather great amount of mitochondria.

Cell Communication↗
PubMed1982

[Membranotoxicity of tumor cells to lymphocytes. Role of homology for IC-subregion of H2-complex].

The object of the research was to examine whether tumor cell membranotoxicity as regards splenocytes depends on the protein synthesis in the latter ones and whether it depends on the similarity or differences in the subregions of H2-complex. As effectors the following tumor cells transplanted in syngeneic mice were used: EL-4 (H-2b), MX-II (H2b), L-1210 (H2d), SA-1 (H2a). As target cells, the splenocytes from the following mice were used: B10/Sn, C57BL/6, B10.A (3R), B10.A (5R), B10.D2, B10.SM, CBA, B10. D2 (R 101), B10.D2 (R 107). It was shown that noncoincidence of the effectors and targets as regards the genetic basis, K, IA, IB, IJ, IE and D-subregions does not lower the maximal membranotoxicity inherent in the entire syngeneic system. Noncoincidence of the effectors and targets as regards the D-terminal of H-2 complex reduces more than 2-fold the effect of tumor cells on splenocytes. Thus, the coincidence of the effectors and targets only as regards the IC-subregion of H-2 complex is enough for attainment of the maximal membranotoxicity of tumor cell as regards splenocytes. It is discussed whether the injury to the target membrane (membrane toxicity) recorded in the research under consideration should be considered as cytotoxic (the target death) or as cytostatic. It is suggested that the phenomenon studied may underlie the immunosuppression due to tumor cells.

Animals↗
PubMed1982

[Role of homology in the JC subregion of the H2 complex in the reciprocal suppression of normal killer and tumor cells].

Attempts have been made to find out 1/whether there is an interaction between normal killers (NK) and tumor cells transplanted in vivo and how both effectors' cytotoxicity against the third participant - NK-sensitive target cells, is affected by the hypothetical interaction; and 2/the implication of H2-complex in the interaction of both the effectors. Use was made of an experimental three-component model in vitro. It included the effector cells of two types. As NK use was made of splenocytes from C57BL/6; CBA; B10; SM; B10.D2; B10.A(3R); B10.A(5R); BALB/C; A/Sn; B10.D2(R107); B.10.D2(R101) mice. Tumor effectors were EL-4 MX-11 (H2b), L-1210 (H2b) and SA-1(H2b) cells transplanted on syngeneic mice. EL-4 cells adapted in culture in vitro were used as standard target cells. Two types of the effector interaction are described. The homology of NK and tumor effector cells in the D-end of H2-complex in the I-C subregion was found to lead to a marked mutual suppression of both the participants with reference to the third component - EL-4 target cells adapted in vitro. The absence of homology in the DC-end of H2-complex provided an opposite effect - summation of cytotoxicity of NK and tumor effector cells against EL-4 target cells. The authors discuss whether the cause of mutual suppression is repaired cytotoxicity (or membrane toxicity) of NK and tumor cells.

Animals↗
PubMed1982

[Activation of the membrane toxicity and cytotoxicity of the tumor cell by leukocyte and fibroblast interferon].

The effect of exogenous interferon on membrane toxicity and cytotoxicity of mouse tumor cells (MX-II, SA-I, thymomas, IAC) was studied with respect to target IAC-I cells. The treatment with leukocyte interferon made tumor cell membrane toxicity rise by 27-40%, while that with fibroblast one by 30-47%. As a result of the treatment with leukocyte interferon, tumor cell cytotoxicity increased by 26-47%. Antiserum against fibroblast interferon reversed its activation effect on tumor cells. It is assumed that the effect described is linked with the increased resistance of tumor cells as regards normal killers under interferon action.

Animals↗