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I Földes

Publications and source records attributed to I Földes.

At least 37 records · Page 2Linked to original sources

Phospholipase C and phospholipase A2 are involved in the antiviral activity of human interferon-alpha.

Treatment of human amniotic cells (UAC) with human interferon-alpha (Hu-IFN alpha) or phorbol myristate acetate (PMA) resulted in translocation of protein kinase C (PK-C) activity from the cytosol fraction to that of the membranes. Analysis of 32P incorporation into phospholipid fractions and studies of alterations in fatty acid content for the major phospholipids of IFN-treated cells suggest that phospholipases C and A2 are activated by Hu-IFN alpha. Addition of neomycin (an inhibitor of phospholipase C), as well as mepacrine (an inhibitor of phospholipase A2) to IFN-treated cells inhibited the antiviral activity of Hu-IFN alpha in the vesicular stomatitis virus (VSV)-UAC system used. These observations indicate that (i) activation of PK-C and (ii) diacylglycerol formation, arachidonic acid and/or lysophosphatidylcholine release are important steps in the mechanism of action of IFN.

Amnion↗

Interferon (IFN)-like antiviral effect is induced by unspecific cross-linking of cell surface receptors.

Treatment of human amniotic cells (UAC) with Cytodex 1 (DEAE-dextran) results in the development of an antiviral state of the cells, as proven by studying (i) the cytopathic effect and (ii) [3H]uridine incorporation into the RNA of vesicular stomatitis virus (VSV) after VSV infection. The same treatment transiently triggers the breakdown of inositol phospholipids and activates the translocation of protein kinase C (PKC). On the basis of these data it can be suggested that cross-linking of cell surface receptors by a solid carrier bearing covalently bound positive charges may result in IFN-like effects.

Antiviral Agents↗

Interferon-inducibility is diminished in tumour-bearing mice.

Inducibility of interferons was studied in tumour-bearing mice. Using five different transplantable tumour-models, diminishing of interferon-inducibility was revealed during tumour progression, irrespectively of the tumour-model used. Diminishing of interferon-inducibility runs parallel with development of the tumours.

Adenocarcinoma↗

Comparison of the effects of peritoneal and spleen cells of syngeneic or allogeneic origin on the take of transplantable murine tumours.

We compared the effects of various potential effector cells of syngeneic or allogeneic origin on the take of a spontaneous adenocarcinoma (SP4) and Lewis lung (LL) carcinoma. As reported earlier, syngeneic resident (non-activated) peritoneal cells (PC) did not inhibit the take of these tumours. On the contrary, transfer of resident PC from allogeneic donors suppressed the tumour take. Syngeneic and allogeneic PC activated by poly I:C or by a combination of indomethacin, poly I:C and Syncumar ("combined treatment") inhibited the tumour take to a similar extent. Syngeneic spleen cells (from untreated mice or from donors underwent "combined treatment") did not inhibit the take of Lewis lung tumour. Transfer of activated allogeneic spleen cells resulted in a stronger inhibition of tumour take than the transfer of resident allogeneic spleen cells.

Acenocoumarol↗

Characterization of activated peritoneal cells inhibiting the take of transplantable murine tumours.

We studied the properties of activated peritoneal cells (PC) inhibiting the take of SP4 spontaneous adenocarcinoma and Lewis lung carcinoma in syngeneic mice. Treatment of the poly I:C activated PC from Balb/c mice suppressing the take of SP4 tumour with anti-asialo GM1 antibody and complement before transfer did not affect their tumour-inhibitory potential. PC from Balb/c nude mice treated with poly I:C also inhibited the take of SP4 tumour. Spleen cells from untreated or poly I:C treated Balb/c and Balb/c nude mice, however, did not inhibit the take of SP4 adenocarcinoma. Treatment of peritoneal cells activated by a combination of poly I:C, indomethacin and Syncumar (referred to as "combined treatment") with anti-asialo GM1 antibody and complement could not, or could only partly abolish their tumour-inhibitory potential. The cells mediating the suppression of the take of Lewis lung tumour proved to be Thy-1,2+/-, Lyt-1-, Lyt 2.2- cells. We conclude that the activated peritoneal cells inhibiting the take of SP4 adenocarcinoma and Lewis lung tumour are different from NK cells, NC cells and LAK cells and represent a distinct antitumoural effector cell population.

Acenocoumarol↗

Enhanced take of spontaneous murine tumors in mice treated with inhibitors of macrophage and/or NK cell function.

Both macrophages and NK cells have been suggested to play a role in recognizing and eliminating early, in situ neoplasms. Therefore we studied the effect of inhibitors of macrophage and/or NK cell function on the take of transplantable spontaneous murine tumors in syngeneic mice. The treatment of animals with trypan blue, a selective inhibitor of macrophage function, decreased considerably the period of latency of BSP3 adenocarcinoma; however, it did not increase the take of SP4, SP82 and SP84 adenocarcinomas. The treatment of recipients with neutral red, a selective inhibitor of NK cell function, enhanced the take of SP4 adenocarcinoma. The treatment of mice with agents depressing both macrophage and NK cell function (silica or carrageenan) decreased the both macrophage and NK cell function (silica or carrageenan) decreased the period of latency and/or increased the take of SP4, SP82 and SP84 adenocarcinomas. Carrageenan or a combined treatment with both trypan blue and neutral red also enhanced the take of BaF1, a benzo(a)pyrene-induced fibrosarcoma. We concluded that both macrophages and NK cells may function as effector cells of an antitumoral surveillance system.

Adenocarcinoma↗

Sulfhydryl groups generated by macrophages into the culture medium.

Previous data showing that thiols can functionally replace macrophages in certain in vitro lymphocyte reactions have raised the possibility that macrophages generate SH groups in the medium. The SH activity of cell-free medium decreases considerably due to auto-oxidation. The presence of macrophages inhibited the spontaneous decrease of SH activity and even increased the number of free SH groups in the culture media. This was designated as SH generation. Resident as well as in vivo stimulated (NaIO4, thioglycollate medium, paraffin oil or BCG) macrophages have nearly the same capacity to generate SH groups when cultured in vitro. The SH-generating ability of macrophages depends on the viability and density of cells, and is greatly influenced by the serum concentration of the media. The majority of SH groups produced by macrophages could be demonstrated as albumin SH groups and proved to be more resistant to autooxidation than non-protein thiols. Moreover albumin could replace whole serum in respect of SH generation. It is suggested that macrophages by generating SH activity, may exert a non-specific helper function to lymphocytes or other cells in their environment.

Albumins↗

Nuclear factor 1 (NF-1) binding sites in the genomes of human oncoviruses: a hypothetic role for reintegrated cellular origins of replication in malignant transformation.

We have found that genomes of human T cell leukemia-lymphoma virus type I (HTLV-I), BK virus (BKV), and a hepatitis B virus (HBV) DNA sequence integrated into DNA of a hepatoma-derived cell line contain binding sites for nuclear factor 1 (NF-1), a cellular protein which binds to adenoviral and putative cellular origins of DNA replication. We suggest that cellular origins of DNA replication acquired by oncoviruses may play a role in malignant transformation after reintegration into the cellular genome by providing new targets for cellular factors initiating DNA replication and by perturbing the temporal order of replication.

Binding Sites↗

Proteoglycan biosynthesis is stimulated by D-penicillamine in chondrifying high density cell cultures.

Chondrifying high density cell cultures of stage 22-24 chick embryo limb bud mesenchyme were treated with 5, 10 and 15 mmol/l D-penicillamine (DPA) for 4 and 6 days. The cultures were analyzed with morphological and biochemical techniques to learn more about the effect of DPA on the metabolism of cartilage glycosaminoglycans (GAGs). Using light and electron microscopic histochemical reactions for GAG, a considerable increase in the intensity of staining of the cartilage matrix could be detected in cultures treated with DPA as compared to the untreated controls. The uronic acid content of the treated cultures was higher than that of the controls. Liquid scintillation measurements and autoradiography revealed that DPA treatment increased the 35S-sulfate into the cultures. These data suggest that DPA - besides its well known inhibitory effect on collagen crosslink formation - alters the metabolism of sulfated GAGs in differentiating cartilage. It is supposed that DPA stimulates the biosynthesis of these macromolecules.

Animals↗

Effect of vitamin D3 and 25 hydroxyvitamin D3 on glycosaminoglycans in micro high density culture.

Vitamin D3 and 25-OH-D3 were tested for their effect on glycosaminoglycan (GAG) production in micro high density cultures of stage 22-24 chicken limb bud mesenchyme. Vitamin D3 (at concentration of 5 x 10(-6)M) and its biologically active metabolite, the 25-OH-D3 (at concentration of 5 x 10(-8)M) stimulated the synthesis of GAGs indicating the increase of radioactive sulfate incorporation and uronic acid content in a dose-dependent way. The findings obtained after the treatment with 25-OH-D3 are comparable with earlier studies performed on chondrocyte cultures (Corvol et al. 1978, 1980), while the results observed after the vitamin D3 treatment are the first indications that vitamin D3 can also influence the cartilage matrix composition.

Animals↗

The effect of ipriflavone treatment on osteoporosis induced by immobilization.

The purpose of these experiments was to study the effect of Ipriflavone (7 isopropoxy-isoflavone) on the osteoporosis induced by immobilization. The immobilization was produced by plaster cast of the right hind limb in young and old rats. Ipriflavone was administered via a gastric tube in a daily dose of 40 mg/kg body weight for 8 weeks. On the basis of histological and histomorphometric examinations of the tibia, results of Ipriflavone treatment are the following: 1) The decrease in the density and volume of spongy trabecules was less apparent in both meta- and diaphysis; 2) The amount of persisting cartilage core and structural rarefication of trabecules were diminished; 3) In the metaphysis osteoblastic activity was considerably enhanced; 4) Bone resorption and cortical thinning were decreased; 5) Bone remodeling was increased subperiosteally and to small extent also endosteally; 6) The treatment did not prevent the development of osteoporosis but significantly diminished it.

Aging↗

Prevalence of HIV-antibodies in patients with haemophilia in Hungary.

Incidence of HIV antibodies have been studied in 617 patients with congenital bleeding disorders. Screening was performed with the Organon ELISA test, repeatedly positive samples were tested with four different confirmatory assays. HIV antibodies were found in 3/356 patients with haemophilia A, 21/114 patients with haemophilia B, 3/123 patients with von Willebrand disease and in 1/24 patients with other types of congenital coagulation disorders. All the 28 seropositive patients were treated with imported coagulation factor, mostly with factor IX concentrates. No patient treated exclusively with nationally produced factor preparations between 1981 and 1985 was found to be anti-HIV positive.

Acquired Immunodeficiency Syndrome↗

Inositol phospholipid turnover and protein kinase C translocation are stimulated by poly(I).poly(C) in human amnion cells (UAC).

Polyinosinic-polycytidylic acid, a potent inducer of inducer of interferon (IFN) production and activator of some IFN-induced enzymes, inhibits [3H]uridine incorporation into the RNA of vesicular stomatitis virus even in the absence of IFN synthesis, transiently triggers the breakdown of inositol phospholipids and activates the translocation of protein kinase C. Since IFNs also have similar activities these results suggest that IFN induction and IFN function are realised through common biochemical pathways.

Amnion↗

Homologies between small nuclear RNAs and LAV/HTLV-III sequences and their possible role in the cytopathic effect of the virus.

The mechanism of action of LAV/HTLV-III resulting in a pronounced cytopathic effect is still unknown. We demonstrate that the long terminal repeat (LTR) sequence and env gene of LAV/HTLV-III contain regions of 70-80% homology and/or complementarity with regions of small nuclear (sn) RNAs U1 and U2. On this basis, we hypothesize that the cytotoxic effect of LAV/HTLV-III is due - at least partly - to the inhibition of processing of cellular hnRNAs by competing for splice junction sites and/or by complexing with U1 and especially U2 RNAs.

Base Sequence↗

A novel approach for understanding the effects of interferons--a working hypothesis.

Experimental results accumulated during the last two decades prove that there are no mechanisms specific for interferon (IFN) action. Thus, IFN effects must be realized through the relatively limited number of metabolic pathways available for cell functions. Triggering the receptor system in association with membrane phospholipid breakdown, which plays an important role in signal transduction for a variety of biologically active substances, is suitable to explain generation of the pleiotropic IFN effects, too. Prevalence of one or the other of the "positive" and "negative" pathways of this signal transducing system depending on various known and up-to-now unknown factors may be responsible for the sometimes contradictory effects of IFNs.

Animals↗