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Biomedical subjects

E Israel

Publications and source records attributed to E Israel.

At least 145 records · Page 8Linked to original sources
PubMed1984

Cefotaxime compared with nafcillin plus tobramycin for serious bacterial infections. A randomized, double-blind trial.

In a prospective, randomized, double-blind study, we compared cefotaxime with nafcillin plus tobramycin in the treatment of serious bacterial infections. Of 195 patients with suspected or proven infections who were not neutropenic, definite bacterial infections were identified in 81; 34 of 38 patients given cefotaxime and 26 of 43 given nafcillin plus tobramycin (p less than 0.01) responded to treatment. The difference in response rates occurred primarily in patients with rapidly fatal underlying disease or with an infection outside the urinary tract. A logistic regression analysis showed that treatment with cefotaxime was still associated with a higher response rate after adjusting for several potential confounding factors. Among patients treated for 3 days or more, our criteria for nephrotoxicity were met in 2 of 68 (2.9%) given cefotaxime and 16 of 57 (28.1%) given nafcillin plus tobramycin (p less than 0.001). Prolongation of the prothrombin time and enterococcal colonization did not occur more frequently with cefotaxime. We conclude that cefotaxime may be more effective and less toxic than nafcillin plus tobramycin for patients with serious bacterial infections.

Adult↗
PubMed1983

Differential susceptibility of avian sarcoma cells derived from different periods of tumor growth to natural killer cell activity.

Tumors which are induced in chickens by avian sarcoma virus usually grow actively for 2 to 3 weeks and then regress. We have cultured tumor cells from each of the active and regression periods of neoplastic growth and compared them in terms of sensitivity to natural killer (NK) activity and to specific cell-mediated cytotoxicity. The results indicate that those cells which derive from regressing sarcomas are sensitive to NK activity but resistant to specific cell-mediated cytolysis. In contrast, tumor cells derived from the period of active neoplastic growth can be lysed effectively in either type of assay, although they do not appear to be as susceptible as do "regressor" cells to the action of NK effectors. The addition of autologous virus to these various reaction mixtures is inhibitory to specific cell-mediated cytotoxicity but not to NK-mediated lysis. These data suggest that NK activity may play an important role in the elimination of tumor cells of the "regressor" phenotype, which otherwise appear to be resistant to immune cytolysis.

Animals↗
PubMed1982

Immune stimulation of sensitized chicken lymphocytes by avian retrovirus proteins.

Peripheral blood lymphocytes of chickens bearing tumours induced by avian sarcoma virus can be specifically stimulated to divide by the crude culture fluids of virus-infected cells. In this communication, we show that relevant antigenic activity apparently resides in each of the internal virus proteins p15 and p27. The ability of infectious culture fluids to be mitogenic for sensitized lymphocytes is greatly reduced following treatment with antibodies specific for either total avian myeloblastosis virus (AMV) protein or for p27.

Alpharetrovirus↗
PubMed1982

Immune selection of tumor cell variants in chickens bearing tumors induced by avian sarcoma virus.

We have compared avian sarcoma cells, cultured from tumors at various stages of growth, in terms of their ability to synthesize infectious progeny virus and to express antigens that are reactive with the sensitized lymphocytes of tumor-bearing hosts. Cell-mediated immunity in chickens bearing tumors induced by avian sarcoma viruses was monitored by each of a target cell cytotoxicity test and an antigen-driven lymphocyte stimulation assay. Our results show that it is only those tumor cells which have been derived from progressively growing neoplasms that are able to synthesize infectious progeny virus and to specifically interact with the sensitized lymphocytes of tumor-bearing hosts. In contrast, cells from regressing tumors do not express relevant antigens to the same extent as do progressors, and they synthesize noninfectious particles only. Experiments on cellular outgrowths, derived from the plating at limited dilution of progressively growing tumor cells, revealed that such producers of defective virus are present at the earliest stages of tumor growth. Both these cells and regressing tumor cells are poorly stained (about 10%) in indirect immunofluorescence tests by antiserum against viral envelope glycoprotein, whereas tumor cells from progressing neoplasms react well (about 60 to 85%). These results suggest that tumor cells which are found in regressing neoplasms are selected out by a functional immune response directed against cells which are efficient producers of progeny virus.

Animals↗
PubMed1982

Further studies on the mitogenic and immune-modulating effects of plasminogen activator.

Plasminogen activator (PA), an enzyme which is secreted in large quantities by certain types of tumour cells, is an apparent lymphocyte mitogen. Treatment of mouse spleen cells with anti-Thy-1.2 serum plus complement prevents responsiveness, indicating that T cells are being stimulated to divide. In addition to the foregoing, we have shown that PA has the capacity to interfere with certain types of cell-mediated cytotoxicity and natural killer cell reactions in which tumour cells are employed as targets. These results suggest that PA may play an immune-modulating role which may be of importance in tumour self-defense.

Animals↗
PubMed1981

Plasminogen activator is an apparent lymphocyte mitogen.

Culture fluids of avian sarcoma virus (ASV)-transformed but not normal chicken embryo cells frequently elicited a mitogenic response in normal avian and murine lymphocytes. We examined the possibility that plasminogen activator (PA) might be responsible for the observed mitogenic effect. PA activity, present in culture medium, was correlated positively with lymphocyte mitogenic capacity. Treatment of cells with phorbol myristate acetate, which elevates PA levels, increased mitogenesis. Similar treatment with dexamethasone, which inhibits PA biosynthesis and/or secretion, reduced lymphocyte mitogenic activity. Addition to culture fluids of either benzamidine or diisopropylfluorophosphate, both specific PA inhibitors, blocked lymphocyte proliferative responsiveness to culture fluids. In contrast, neither epsilon-amino-caproic acid nor trasylol, which inhibits plasmin esterase activity but not PA, abrogated lymphocyte responsiveness. Furthermore, purified urokinase, an enzyme of similar substrate specificity to PA, had lymphocyte stimulatory activity. These results strongly suggest that PA can function as a lymphocyte mitogen.

Animals↗
PubMed1980

Viral inhibition of lymphocyte mitogenesis. I. Evidence for the nonspecificity of the effect.

We have investigated the mechanism(s) whereby virus particles, when co-incubated with lymphocytes, are able to abrogate mitogen- and alloantigen-driven cell proliferation. Our data indicate that this inhibition is entirely nonspecific with regard to its induction; similar results can be obtained by using any of several different types of infectious virus particles or viruses whose infectivity had been destroyed by irradiation with ultraviolet light. Furthermore, we show that plasma membranes vesicles, which approximate viruses in size, and which are derived from normal cells, can also impede lymphocyte proliferative responsiveness. In the mixed lymphocyte culture (MLC) reaction, the inhibitory effect is apparently due to the action of viruseith virus can inhibit the mitogen-induced proliferation of resh syngeneic spleen cells, even if added to the latter at a ratio as low as 1:250. These results suggest that virus particles induce the activation of suppressor lymphocytes which in turn act on those cells which would otherwise be responsive in mitogenesis assays and in the MLC.

Animals↗
PubMed1980

Non-specific inhibition by virus particles of human lymphocytes mitogenesis.

Many different types of virus particles including avian retroviruses, Friend leukaemia virus and Sendai virus are able, when coincubated with human peripheral blood lymphocytes in the presence of mitogens or alloantigens, to inhibit the usual proliferative responses that normally ensue. These effects are independent of infection and can be obtained using u.v.-inactivated viruses as well as virus-lymphocyte combinations which are non-physiological in nature. Lymphocytes which are preincubated with viruses for as little as 5 min, and then washed free of unbound virus, are significantly impaired in terms of ability to react to mitogenic stimulus. These events may be mediated, in part at least, by the virus-induced elaboration by mononuclear cells of a factor with lymphocyte inhibitory potential.

Friend murine leukemia virus↗
PubMed1980

Viral abrogation of lymphocyte mitogenesis: induction of a soluble factor inhibitory to cellular proliferation.

PHA and Con A-driven mitogenesis of mouse C3H lymphocytes can be inhibited by co-incubation with a variety of different virus particles. These effects appear independent of infection, and can be obtained using UV-inactivated virus. Viruses may be added to spleen cell cultures as late as 46 h after co-incubation with mitogen, and still achieve significant inhibition of proliferative responsiveness. The described inhibition is apparently mediated, in part at least, by a soluble factor which is induced in splenic cultures following interaction with virus particles. This factor is apparently a product of macrophages. It does not posess interferon activity, but does have the ability to inhibit lectin- and alloantigen-driven mitogenesis, as measured in fresh cultures of splenic lymphocytes and in the mixed lymphocyte culture (MLC) reaction, respectively. Moreover, addition of virus to splenic cultures can apparently activate suppressor lymphocytes with the ability to inhibit proliferative responsiveness of fresh lymphocyte suspensions in the presence of Con A.

Animals↗
PubMed1979

Decreased production of transforming virus and altered antigenic behaviour in cultured avian sarcoma cells.

Tumours induced in chickens by inoculation of avian sarcoma viruses are frequently capable of undergoing spontaneous regression. It is only those tumour cells which have been derived from progressively growing neoplasms that are able to produce transforming progeny virus in vitro and to shed into the culture medium antigens which are specifically reactive with the peripheral lymphocytes of sarcoma-bearing hosts. Following multiple passages and extended growth in culture, however, the ability of these tumour cell fluids to stimulate the lymphocytes of sensitized hosts diminishes in concert with the declining capacity of these cells to continue to synthesize fully transforming progeny virus. In certain instances, however, aged tumour cells are able to synthesize particles which contain the enzyme RNA-dependent DNA polymerase yet lack detectable envelope glycoprotein.

Animals↗
PubMed1979

Non-specific effects of avian retrovirus co-incubation on lymphocyte function: abrogation of antigen- and mitogen-induced proliferative responsiveness.

Peripheral blood lymphocytes from chickens bearing tumours induced by avian retroviruses can be stimulated to divide by group-specific antigens present in supernatant fluids of avian retrovirus-infected but not normal chicken embryo fibroblast (CEF) cells. Centrifugation studies revealed that the relevant antigenic activity is non-virion in nature. Indeed, the presence of avian retrovirus particles was found to be inhibitory to the capacity of sensitized lymphocytes to be stimulated in this antigen-driven blastogenesis assay. Similar results were obtained in lymphocyte mitogenesis experiments in which any of peripheral chicken lymphocytes or mouse splenic, lymph node or thymic lymphocytes were co-incubated with either concanavalin A or phytohaemagglutinin in the presence of numerous types of virus particles. This inhibitory effect was not due to infection of lymphocytes by the viruses tested, and was obtained in the case of lymphocyte-virus combinations for which the cells lacked the surface receptors required for viral entry. Virus could be added to lymphocyte cultures as late as 26 h after co-incubation with mitogen, and still inhibit the usual mitogenic response. In addition, co-addition of virus to lymphocytes in the presence of concanavalin A was found to block the capping of ligand-bound receptors which normally ensues. Pre-added virus did not, however, affect the ability of lectins to bind to cells.

Alpharetrovirus↗
PubMed1978

Enhancement of avian sarcoma virus-induced tumor growth after pretreatment with BCG.

Pretreatment of chickens with BCG 1 week before inoculation with avian sarcoma virus had a stimulatory effect on virus-induced tumor growth in 15 of 17 cases tested. This outcome was dependent upon the injection of both BCG and the oncogenic agent into the same wing web. Injection of BCG into the wing web contralateral to that used for virus inoculation or injection of a subcellular fraction of BCG into the same wing web did not affect tumor development. Administration of BCG also gave rise to heightened levels of tumor-associated, cell-mediated immunity, both on the part of chickens which received a subsequent injection of oncogenic virus as well as normal, BCG-inoculated controls.

Animals↗
PubMed1978

Effect of glucosamine on virus production and antigen expression in avian sarcoma virus-transformed cells.

Treatment by glucosamine of avian sarcoma virus-transformed chicken embryo fibroblast (CEF) cells completely inhibited the formation of progeny-transforming virus particles. Such cells, however, could continue to synthesize non-infectious physical particles containing both viral RNA and the enzyme RNA-dependent DNA polymerase if glucosamine exposure was performed in the presence of glucose. Glucosamine treatment was found to affect antigenic expression in transformed CEF as measured by an indirect immunofluorescence test. Inhibition to a far lesser extent was observed when a lymphocyte stimulation assay for the detection of cell-mediated immunity was used in this system.

Alpharetrovirus↗