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Biomedical subjects

A M LERNER

Publications and source records attributed to A M LERNER.

At least 19 recordsLinked to original sources

REOVIRUS HEMAGGLUTINATION: INHIBITION BY N-ACETYL-D-GLUCOSAMINE.

Purified reoviruses types 1, 2, and 3 were specifically inhibited in their hemagglutination of human erythrocytes by 250 micromoles or more of N-acetyl-D-glucosamine but not by over 20 other sugars tested. N-acetyl-D-glucosamine inhibited reovirus hemaglutination by binding to capsid virus; it did not attach to the erythrocytes. It is possible that reovirus hemagglutination involves union between N-acetyl-D-glucosamine on the surface of the red cell and the glycoprotein of the virus coat.

Acetylglucosamine↗

NEW VIRAL EXANTHEMS.

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Adenoviridae Infections↗

RIBOSOMAL RNA IN THE DEVELOPING CHICK EMBRYO.

Developing chick embryos from the stage of primitive-streak formation make ribosomal (28S and 16S) RNA. The size and composition of the RNA appears to be constant throughout the first 7 days of development.

Animals↗

Age and susceptibility of mice to Coxsackie A viruses.

Mice varying in age from 1 day to 8 months were inoculated intraperitoneally with Coxsackie A virus, type 9 and studies were made of the quantity of virus in striated muscle and myocardium, the presence of neutralizing antibody in the serum, and the pathological changes in the tissues. The hind limbs of young (1- to 20-day-old) mice yielded high titers of virus and showed diffuse myositis, whereas only low yields of virus and focal myositis were obtained in older mice. In the 20-day-old mice the skeletal lesions were not accompanied by manifest symptoms and histologically showed evidence of regeneration progressing from the 3rd to the 11th day after inoculation. Older mice showed no symptoms and only focal myositis and low yields of virus were found in their hind limbs. Coxsackie A9 virus replicated to relatively low titers in the hearts of young (1- to 40-day-old) mice without producing any demonstrable lesions whereas frank myocarditis with high yields of virus were demonstrated in mice infected at 8 months of age. The data suggest that at least for the 2 strains used, the adult mouse should be considered susceptible to subclinical infection with Coxsackie A9 virus. Neither subclinical infection, nor antibody formation was demonstrable in young adult mice inoculated with a strain of Coxsackie A4 virus.

Aging↗