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Biomedical subjects

A Kirn

Publications and source records attributed to A Kirn.

At least 109 records · Page 6Linked to original sources
PubMed1983

[Isolation of 503 strains of virus in meningeal syndromes. Virologic and epidemiologic study].

An epidemiological and virological study on meningitis in Alsace during the 13-year period 1968-1981 is reported. 503 viruses isolated were associated with the diagnosis of meningitis. The Echovirus type 30 accounted for 48 p. 100 of the cases, the mumps virus of 12 p. 100. The remarkable high incidence of Echo 30 virus-associated cases is related to three outbreaks which occurred in Alsace during the summers of 1968, 1975 and 1980. Children below 12 years of age are the most sensitive population and particularly boys who made up 2/3 of the number of cases.

Adolescent↗
PubMed1982

Protective effect of colectomy in frog virus 3 hepatitis of rats: possible role of endotoxin.

Four to six days after colectomy, rats resisted a challenge of frog virus 3 that in sham-operated animals led to lethal hepatitis. Furthermore, the beneficial effect of colectomy was lost after intravenous administration of a dose of bacterial endotoxin as small as 0.01 100% lethal dose. The protection was related to neither a different distribution of the virus in body organs nor a stimulation of the reticuloendothelial system. The virus-induced early events--destruction of liver sinusoidal cells with leakage of cathepsin D into serum and inhibition of liver macromolecular synthesis--evolved similarly in both groups of rats. After an identical consumption of complement at the beginning of infection, a renewal in complement activity in the protected rats contrasted with an increasing deficiency in the control animals. The protective role of colectomy seems to be related to the suppression of the main source of bacterial endotoxin.

Animals↗
PubMed1982

Localization by autoradiography of viral proteins in the parenchymal cells of the liver during frog virus 3 induced hepatitis of mice.

Frog virus 3 inoculated into mice induces an acute degenerative hepatitis. This hepatitis is of toxic origin since the virus is unable to multiply at 37 degrees C. The Kupffer cells, which are the target cells for FV3, reveal the presence of viral particles, viral DNA and proteins. Although the hepatocytes present early and drastic nuclear lesions, viral particles were never observed in these cells. Viral proteins however but not DNA, could be found inside parenchymal cells.

Animals↗
PubMed1981

[Response of splenic lymphocytes to phytohemagglutinin and bacterial lipopolysaccharide in mice, sensitive and resistant to mouse hepatitis virus 3 (MHV3)].

The responsiveness of splenic cells to phytohemagglutinin but not to bacterial endotoxin was inhibited during MHV3 infection of both sensitive (C57Bl6) and resistant (A/J) Mice. This result could be interpreted as the consequence of an inhibition that selectively affects the T lymphocytes during infection. In C57Bl6 sensitive Mice the inhibition could be a consequence of the destruction of splenic T lymphocytes. In A/J resistant Mice, no splenic lesions have been observed; therefore another mechanism must be considered in order to explain the inhibition of the responsiveness of splenic cells to phytohemagglutinin.

Animals↗
PubMed1981

Frog virus 3 induces a fatal hepatitis in rats.

To define its pathogenesis, the acute degenerative hepatitis caused by frog virus 3 (FV3) has been reproduced in the rat, thus facilitating a greater number of biologic explorations than in the mouse. The histologic and ultrastructural study proves a massive hepatocellular necrosis perfectly compatible with the fatal outcome of the illness 30 hours after the inoculation of one LD100. Critical analysis of the FV3 rat hepatitis induces us to advance three arguments for excluding the direct role of the virus in hepatocytolysis. (1) The hepatocyte is neither the sole nor the first intrahepatic target of the virus. The endothelial barrier and especially the Kupffer cells are completely necrosed several hours prior to the appearance of the first signs of parenchymal cell disturbances. Morphologic observations and, in particular, the evolution in the site and chronology of the cytolysis are confirmed by the variation in the activity of cathepsin D, glutamic pyruvic transaminase, and lactic dehydrogenase in serum. (2) There is a close correlation between the structural alterations in the hepatocyte nuclei and the inhibition in the synthesis of the liver macromolecules. But the discovery of a rat strain sensitive to the virus and another more resistant strain provides evidence that there is no relationship between the sensitivity to the lethal power of the FV3 and the metabolic disorders. (3) The ways in which the FV3 spreads throughout the organism do not explain why the liver is the sole organ attacked. A second etiopathogenic factor, only found in the liver, must be invoked. The possible role of the plasma complement, strongly activated, is suggested, along with that of other toxic substances which can no longer be cleared. The metabolic inhibition directly connected with the FV3 would thus result not in producing the hepatocytolysis but in rendering any cellular regeneration impossible.

Animals↗
PubMed1980

[Isolation and culture of human Kupffer cells].

The dissociation of human adult liver parenchyma by collagenase followed by cell separation with centrifugal elutriation allows the Kupffer cells to be isolated. These cells, which may be maintained in culture, retain their main morphological and functional features.

Cell Separation↗