The presence of a plasmid harboring a gene for Cd2+ resistance led to markedly reduced Cd2+ uptake via the energy-dependent Mn2+ transport system in Staphylococcus aureus strain 17810R. Cd2+ uptake by the resistant strain via this high-affinity system was seen only at very low Cd2+ concentrations. At high concentrations, Cd2+ was taken up by the resistant strain via a different low-affinity uptake system. Cd2+ uptake via this system was energy dependent but was not blocked by Mn2+. Loss of the plasmid from the resistant strain resulted in Cd2+ sensitivity and unblocking of Cd2+ transport via the Mn2+ carrier in the plasmidless derivative strain 17810S. The energy-dependent Cd2+ uptake by the sensitive strain was inhibited by Mn2+ with kinetics indicating competitive inhibition. It is suggested that the second, low-affinity uptake system for Cd2+ in the resistant strain is the energy-dependent cadmium/proton antiporter, which at low Cd2+ concentrations functions in net Cd2+ efflux.

Biological Transport, Active↗

PubMed1981

Energy-dependent efflux of cadmium coded by a plasmid resistance determinant in Staphylococcus aureus.

Resistance of Staphylococcus aureus strain 17810R to Cd2+ appears to be due to a plasmid-coded Cd2+ efflux system. Complete efflux of Cd2+ after transfer of preloaded cells into Cd2+-free medium occurred in the resistant strain 17810R, but not in the plasmidless derivative strain 17810S. Net efflux was blocked by 2,4-dinitrophenol, N,N,-dicyclohexylcarbodiimide (DCCD), and incubation at 4 degrees C. The inhibition of Cd2+ efflux by DCCD paralleled a stimulation of net uptake in the resistant cells by this agent. Cd2+ efflux by the resistant strain was accompanied by a reversal of inhibition of respiration, whereas in the sensitive strain, inhibition of respiration was not reversed after transfer to Cd2+-free medium. Net Cd2+ uptake by strain 17810R was inhibited by p-chloromercuribenzoate. In Cd2+ contrast, Cd2+ uptake by the plasmidless strain 17810S was affected neither by p-chloromercuribenzoate nor by DCCD when added alone, but was blocked by a combination of these two agents. Valinomycin had no effect on the reduced Cd2+ uptake by the resistant strain, whereas nigericin stimulated uptake to values comparable to those of the untreated sensitive cells. With sensitive cells, valinomycin reduced Cd2+ uptake by about 50%, whereas nigericin was without effect. A possible mechanism of Cd2+ movements in both strains is discussed.

Biological Transport, Active↗

PubMed1981

[Comparison of the thermostability of Newcastle disease virus strains isolated in Slovakia].

Reference strains of Newcastle disease virus of different virulence (two lentogenic, two mesogenic and three velogenic), isolated in Czechoslovakia and other countries, were compared with 11 field strains isolated in Slovakia in 1973, 1977, 1979 and 1980 as to the stability of their infectivity for cell cultures and as to their hemagglutination activity at a temperature of 56 degrees C for 120 minutes. The inactivation curves indicate that ten strains belong to the group of velogenic viruses and one of them is lentogenic. Although the data on hemagglutinin thermostability and infectivity do not suffice to characterize the virus strain, it is possible, by comparing the inactivation curves determined by the described method, to differentiate the field strains of Newcastle disease virus as lentogenic, mesogenic and velogenic. Some instability of the relationship between the thermostability and virulence of the virus is ascribed to the heterogeneity of the virus population.

Animals↗

PubMed1980

[Early relaparotomy].

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Abdomen↗

PubMed1980

Epilepsy and complication after craniocerebral traumas.

Three hundred and seventy-two patients aged from 24-80 years were examined 10-15 years after past craniocerebral trauma. Of that number 355 subjects had concussion and 17 subjects brain contusion. Posttraumatic epilepsy was diagnosed by 8 cases (2.15%) only. It affected 4 females, aged from 40-60 years, and 3 males aged 30-48 years after the brain concussion, as well as 1 man, 30 years old, after the brain contusion. That first epileptic attack in 4 cases occurred after the lapse of 1-2 years, in 3 persons after the lapse of 6-10 months, and 1 patient having had brain contusion after 4 months. All posttraumatic patients were treated prophylactically with phenobarbital 0.1 twice a day for a period of several weeks.

Adult↗

PubMed1980