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Biomedical subjects

A Kirn

Publications and source records attributed to A Kirn.

At least 127 records · Page 7Linked to original sources
PubMed1980

Induction of intranuclear microtubules in chick embryo fibroblasts by frog virus 3.

Intranuclear microtubules appear in chick embryo fibroblasts upon infection with Frog Virus 3 (FV 3). Both the diameter and the annular shape of the microtubule profiles, established from electron microscopic observations using a goniometer, suggest that they are identical to naturally occurring cytoplasmic microtubules. Furthermore, the use of vinblastine allowed demonstration of the tubulin composition of the intranuclear microtubules.

Animals↗
PubMed1979

[Worldwide eradication of smallpox or from Sarah Nelmes to Ali Maow Maalin].

It cannot be disputed that the WHO plan for the eradication of smallpox has had considerable success. There is no endemic smallpox any longer in the world. Nevertheless caution is advised and continued supervision must not be neglected. There are still countries where supervision is not satisfactory, there is uncertainty about animal reservoirs and it should be assumed from the beginning that up to the present no epidemic disease could be completely eradicated. For this reason it is inevitable that supplies of vaccine should be available. A vaccine from heat sensitive strains is offered which is obtained from cell cultures.

Animals↗
PubMed1979

Effect of cell-mediated immune factors on the replication of an attenuated temperature-sensitive mutant of vaccinia virus.

Studies of the in vivo multiplication of an attenuated temperature-sensitive strain of vaccinia virus (ts2) indicated that temperature sensitivity alone could not account for the attenuation. Immunodepressive treatment of intracerebrally inoculated mice had a dramatic stimulatory effect on the multiplication of the attenuated strain and suggested that establishment of ts2 infection in the mice was hindered by host defense mechanisms mediated by cellular elements. Experiments carried out in vitro with the 51Cr release assay showed that cells infected with the ts2 mutant represented more susceptible targets to the cytotoxic action of immune spleen cells than cells infected with the parent vaccinia strain. Moreover, it appeared that ts2 replication, compared with wild-type replication in vitro, was more inhibited by the immune spleen cells. Although this work did not evaluate the role of specifically sensitized lymphocytes within the lesions, indirect evidence suggests that lymphocytes could cause a more effective halt in ts2 virus multiplication than in wild-type multiplication.

Animals↗
PubMed1979

[Protection of mice with bacterial phospholipids against the lethal effect of Frog Virus 3 (FV 3) (author's transl)].

A bacterial phospholipid extract (EBP) inoculated intraveinously at a dose of 1 mg/25 g body weight 30 hours before infection protects mice against the lethal effect of Frog Virus 3 (FV 3). The anti-FV 3 resistance produced by EBP requires protein synthesis during the period of pretreatment. The treatment with the bacterial extract has no effect on the inhibition of the macromolecular synthesis of the liver (RNA and DNA) which is observed at the beginning of the infection. However 48 hours after FV 3 infection, there is a notable stimulation of DNA synthesis which probably corresponds to liver regeneration.

Animals↗
PubMed1979

[Effect of a water-soluble derivative of silymarin on morphological and functional alterations of mouse hepatocytes induced by Frog Virus 3 (author's transl)].

Pretreatment of mice with silymarin dihemisuccinate sodium salt (SHS-Na) 300 mg/kg 24 and 16 h before infection completely protected against the lethal effect of Frog Virus 3 (FV3). After the inoculation of 1 LD100 of virus it could be shown that: a) the same amount of radioactively labelled virus was found in the liver of control and SHS-Na treated animals, b) in SHS-Na pretreated animals the shut-off of macromolecular syntheses in the liver was considerably less extensive, c) the histological changes in the hepatocyte nuclei were attenuated in SHS-Na pretreated animals and the serum titer of the transaminases did no increase, d) in SHS-Na pretreated mice there were only limited functional alterations of the sinusoidal cells as studied by carbon phagocytosis and the serum titer of the lysosomal enzymes was only slightly modified, e) inhibition of protein synthesis during the period of pretreatment with SHS-Na did not decrease the level of protection. These results allow us to conclude that SHS-Na exerts its protective effect on the liver and that sinusoidal cells are most likely involved in this protection.

Animals↗
PubMed1978

In vitro growth characteristics and heterogeneity of mouse hepatitis virus type 3.

The in vitro virus yield of MHV3 reached 10(7) PFU/ml in mouse DBT cells infected with a virus suspension in HEPES-buffered medium containing DEAE-dextran. The virus titer was 10(6) PFU/ml in the presence of 10 micrograms actinomycin D/ml MHV3 growth in DBT cells gave three peaks of density (1.10--1.14 g/cm3, 1.18--1.20 g/cm3, and 1.25--1.31 g/cm3) in sucrose gradients. All these peaks retained infectivity.

Cell Line↗
PubMed1978

Host range restriction of vaccinia virus in Chinese hamster ovary cells: relationship to shutoff of protein synthesis.

Chinese hamster ovary cells were found to be nonpermissive for vaccinia virus. Although early virus-induced events occurred in these cells (RNA and polypeptide synthesis), subsequent events appeared to be prevented by a very rapid and nonselective shutoff of protein synthesis. Within less than 2 h after infection, both host and viral protein syntheses were arrested. At low multiplicities of infection, inhibition of RNA synthesis with cordycepin resulted in failure of the virus to block protein synthesis. Moreover, infection of the cells in the presence of cycloheximide prevented the immediate onset of shutoff after reversal of cycloheximide. Inactivation of virus particles by UV irradiation also impaired the capacity of the virus to inhibit protein synthesis. These results suggested that an early vaccinia virus-coded product was implicated in the shutoff of protein synthesis. Either the nonpermissive Chinese hamster ovary cells were more sensitive to this inhibition than permissive cells, or a regulatory control of the vaccinia shutoff function was defective.

Cell Line↗
PubMed1978

Phagocytic properties displayed by mouse hepatocytes after virus induced damage of the sinusoidal lining.

Frog virus 3 (FV 3) inoculated intravenously into mice damages sinusoidal cells and produces a decrease in the carbon uptake capacity of the liver. Histological and ultrastructural examinations have shown that in FV 3 infected animals part of the inoculated carbon is taken up by the hepatocytes and can be located inside cytoplasmic vesicles or dense bodies. The hepatocytes are also able to phagocyte latex particles of 312 nm in diameter. These observations demonstrate that once the Kupffer cells and the endothelial lining are damaged, hepatocytes can display phagocytic properties.

Animals↗