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Biomedical subjects

F M HARDY

Publications and source records attributed to F M HARDY.

10 recordsLinked to original sources
PubMed1965

LIPID INCLUSIONS IN L CELLS ASSOCIATED WITH VENEZUELAN EQUINE ENCEPHALOMYELITIS VIRUS INFECTION.

Hardy, Frank M. (Fort Detrick, Frederick, Md.), and David Arbiter. Lipid inclusions in L cells associated with Venezuelan equine encephalomyelitis virus infection. J. Bacteriol. 89:1101-1103. 1965.-Venezuelan equine encephalomyelitis (VEE) virus has been shown to induce changes of lipid components within the L cell. Lipid inclusions in the form of dark granular bodies were observed in the L cell after aqueous osmium tetroxide fixation and Sudan black staining. Microscopic examination of cells as early as 8 hr after infection with VEE virus showed an increase in the concentration of these inclusions within the cytoplasm. According to various lipid solubility criteria, the inclusions were considered a combination of heterogeneous phospholipids.

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PubMed1962

Antenatal care.

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PubMed1961

Growth of Venezuelan equine encephalomyelitis virus in L cells. II. Growth in submerged culture.

Hardy, Frank M. (U. S. Army Chemical Corps, Fort Detrick, Frederick, Maryland), and Arthur Brown. Growth of Venezuelan equine encephalomyelitis virus in L cells. II. Growth in submerged culture. J. Bacteriol. 82:449-457. 1961.-The detailed kinetics of Venezuelan equine encephalomyelitis virus multiplication and release and the progressive cell death due to the virus infection were studied in a uniformly susceptible L cell population. The adsorption phase was complete in approximately 15 min with multiplicities of 1, 10, and 100 MICLD(50). An eclipse phase showing the disappearance of some of the infectious virus activity lasted between 3 and 4 hr. An exponential increase of cell-associated and free virus then occurred until peak titer was reached (16 to 18 hr). Relatively constant titers of cell-associated or free virus were obtained from the time peak titer was attained until the 52nd hour of incubation. At that time the cell-associated titer declined more rapidly than the free virus titer. These constant titers, however, masked a continued production and release of new infectious virus. By viable and nonviable cell counts, it was determined that cell death occurred relatively late in the phase of constant growth and release.

Animals↗