[Morphological changes in the pancreas in Zollinger-Ellison syndrome].
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Biomedical subjects
Publications and source records attributed to K Apostolov.
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The effect of Sindbis virus on cell leakiness, as measured by chromium release, and on the fatty acids in chick embryo fibroblasts and Vero cells was studied. The appearance of the cytopathic effect in both cell types coincided with virus replication, increased cell leakiness and relative increase in saturated eighteen carbon fatty acid (C18:0, stearic acid) compared to the eighteen carbon unsaturated fatty acids (C18UFA). It is postulated that the increase in cell leakiness and the appearance of cytopathic effect could be the result of a physical change in the lipids of the cell membrane brought about by the increase in the saturation of the eighteen carbon fatty acids.
Diptheria toxin (DT) reversibly increases the saturation of the long-chain C18 fatty acids (C18FA) in concentrations which are at least 100-fold smaller than the concentrations which completely inhibit host cell protein synthesis. The concentrations required for induction of the increase in the saturation of the C18FA in fibroblasts are 100-fold smaller than the concentrations for the epithelial cells. The increase in saturation of the C18FA was proportional to the concentration of DT. A cytopathic effect appeared with DT concentrations which induced a near-maximal increase in the saturation of the C18FA, but the cells remained viable. However, at very high concentrations of DT and depending on the type of cell, there was no change in the fatty acids, and the treated cells disintegrated. Interferon, which also induces a reversible increase in the saturation of the C18FA (K. Apostolov and W. Barker, FEBS Lett. 126:261-264, 1981), produces a cumulative effect when used in conjunction with DT. This additive effect of DT and interferon is discussed in the light of other similar biological activities of these agents.
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Chick embryo fibroblasts (CEF) infected with virulent strains of Newcastle disease virus (NDV) showed a dramatic increase in total unsaturated fatty acids (UFA). This increase was not seen in cells infected with the avirulent strains of NDV, Sendai virus or influenza A (PR8). The virions of the virulent strains of NDV harvested from the chorioallantoic cavity also had a higher UFA content compared to the avirulent ones. The kinetics of UFA increase in the virulent strains could be correlated with published data on the kinetics of RNA and protein synthesis inhibition, polykaryon formation and membrane permeability changes.
Treatment of Newcastle disease virus with iodine inhibits haemolysis and infectivity, but has no effect on haemagglutination. This is shown to be concurrent with the incorporation of iodine in the hydrocarbon chain of fatty acyl residues of the viral membrane lipid. It is concluded that iodine incorporation, by reducing membrane fluidity, is responsible for these biological phenomena.
Lugol's solution destroys the biological activities of Newcastle disease virus (NDV) after 15 s incubation at 37 degrees C. The rates of inactivation are slower at lower temperatures and at acid pH. At 4 degrees C and pH 5.8, the functions associated with the virus membrane, (haemolysis (HL), cell fusion and infectivity) are inactivated within 32 min, while haemagglutination (HA) and neuraminidase (N) are resistant to inactivation for several hours. Adjustment of NDV, Sendai and influenza A virus allantoic harvests to pH 5.8 and subsequent treatment with undiluted Lugol's solution (pH 5.8) for 15 min has a minimal effect on HA but results in complete loss of infectivity. It is suggested that iodination could be a useful method for vaccine production with membrane-bound viruses. It is postulated that the separation and dissociation of the membrane-associated properties of paramyxoviruses from the glycoprotein functions is due to the higher affinity of iodine for the lipids. Iodine could react with the carbon-carbon double bond (C=C) of the unsaturated fatty acids. This could lead to a change in the physical properties of the lipids and membrane immobilization.
The capacity of paramyxoviruses for haemolysis (hl) is enhanced after treatment with physical agents and complement (C'). Bivalent cations in the medium inhibit HL. The inhibition is proportional to the molar concentrations, and is graded Ba++ greater than Ca++ greater than Mg++. Substitution of the bivalent cations with K+ and re-incubation leads to reappearance of HL, but in reverse order. It is postulated that bivalent cations inhibit HL mainly by stabilising the virus membrane integrated into the erythrocyte membrane and slowing down the permeability rates. This inhibition is removed on substitution with monovalent cations. The bivalent cations also reversibly inhibit the permeability of the transferred C' lesion.
The events of fusion of 11- and 16-day embryonic mouse liver erythroblasts induced by Sendai virus (SV) were followed with the scanning electron microscope (SEM). Erythroid precursors incubated with the virus showed numerous 'pores' on the cell membrane. The cell fusion began with the appearance of a fine 'meshwork' structure between the adjacent cells, followed by a gradual formation of a common cell membrane and terminated with the appearance of polykaryons, in which the nuclei were easily recognized when located in the vicinity of the polykaryon membrane. There was no difference in the process of fusion between erythroblasts at identical and those at different stages of maturation.
The ultrastructural events of the interaction of Sendai virus (SV) with fetal mouse erythroid precursors, and SV-induced fusion of erythroid precursors at different maturation stages are described. SV was shown to affect the erythroid nuclei causing interruption of the nuclear membrane, enlargement of the nucleolus and nuclear fusion. SV induced fusion also between dividing and non-dividing cells.
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Pre-treatment of Newcastle disease virus (NDV) with fresh human plasma enhances its haemolytic (HL) capacity by several factors. The effect is due to complement activation by the heterophile anti-chick antibody present in human plasma. All the adult human plasmas tested were effective, also 91/100 human cord blood sera. The antibody was mainly of the IgM class. The enhanced HL was due to integration and transference of the complement 'holed' virus envelope membrane and subsequent leakage of haemoglobin. High concentration of activated complement destroys the integrity of the virus enevelope. Treatment of chick erythrocytes and fibroblasts with human plasma also produced lysis of the cells.
Triais with a total of 240 cows were carried out. The animals were given 30 g DL-methionine each per day. Results showed that the infusoria count per one cu.cm of rumen content in lactating cows that had been given methionine at the rate of 30 g daily was 137013, while in the control animals it was 76431. The amount of lipid matter rose by 0.4 per cent in the controls in the course of the first 90 days of the lactation period. The milk yield of cows that received methionine also rose by 16 per cent, on an average, as calculated in terms of 4 per cent butterfat content for 24-hour period up to the third month of lactation. DL-methinionine in the diet of cows for the first months of lactation leads to grater amounts of milk of higher quality as well as to improving the health of the animals.