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R H Kimberlin

Publications and source records attributed to R H Kimberlin.

At least 73 records · Page 4Linked to original sources
PubMed1976

Search for scrapie-specific RNA and attempts to detect an infectious DNA or RNA.

Preparations of in vivo labelled RNA from normal and scrapie infected mouse brains were fractionated by polyacrylamide gel electrophoresis. No appreciable differences were detected between the two preparations. The biological activity of preparations of RNA and DNA from scrapie brain was also examined. In each case the nucleic acid was obtained by one method envolving the use of phenol and one without phenol. Attempts were made to bind the nucleic acid to normal membrane by three different methods. In no instance was a single case of scrapie obtained by inoculating nucleic acid extracts from scrapie brain either alone or associated with normal membranes. It is concluded that a putative scrapie-specific nucleic acid must either be present in scrapie brain in such an unusual from that it is not extracted readily by methods suitable for the preparation of most virus nucleic acids; or, if it is extracted, that it has no detectable biological activity. In either case, the scrapie agent differs substantially in its properties from the plant viroids.

Animals↗
PubMed1976

Motor activity changes in scrapie-affected mice.

Measurements of spontaneous motor activity using Animex equipment have been made throughout the incubation period in mice developing scrapie. A progressive fall in activity has been noted from an early stage in the disease process well before clinical signs of scrapie were evident. The initial fall was followed by an upsurge in activity at about the time when clinical signs of disease develop.

Animals↗
PubMed1975

Comparison of scrapie and transmissible mink encephalopathy in hamsters. II. Clinical signs, pathology, and pathogenesis.

Scrapie and transmissible mink encephalopathy were studied in hamsters; clinical signs, pathology, and the replication of the agents of each disease in brain and spleen were compared. The most noticeable clinical sign in scrapie-affected hamsters was a distinct cerebellar ataxia beginning 16 weeks after inoculation. Ataxia was not prominent in animals affected with transmissible mink encephalopathy; these animals gradually became more and more lethargic. The pathology in the central nervous system in both diseases consisted of astrocytic hypertrophy, microvacuolation of the neuropil, and neuronal degeneration. The scrapie agent appeared to have a greater effect on nuclear masses, especially those present in brain stem and the central white matter of the cerebellum. The earliest lesions in both diseases were detected near pia arachnoid surfaces and adjacent to the ventricular system. These initial sites of involvement suggest that the cerebrospinal fluid may be an important route by which inocula are disseminated to susceptible cells after intracerebral inoculation. Both agents multiplied rapidly in brain, reaching titers greater than 10-8 ld-50/0.05 ml before the onset of clinical signs. Titers in spleen were 4-6 logs lower than titers in brain at every point measured during the asymptomatic or clinical course of disease.

Animals↗
PubMed1975

Comparison of scrapie and transmissible mink encephalopathy in hamsters. I. Biochemical studies of brain during development of disease.

A series of 15 different biochemical measurements were made on brains taken at stages throughout the development of scrapie and of transmissible mink encephalopathy in hamsters. With both diseases biochemical abnormalities were found only after the development of early histologic lesions, when animals showed clinical signs of disease. Changes were recorded in body weight, in the activities of six glycosidases, and the rates of incorporation of DNA and of glycoprotein precursors. The profiles of changes in hamster brain were almost indistinguishable,qualitatively and quantitatively, in the two diseases, an observation suggesting a close similarity in the way both disease-producing agents interact with this particular host species, . However, there were some major differences between the profile of changes in hamster scrapie and that previously observed in mouse scrapie. Thus it would appear that many of the well-characterized abnormalities of mouse scrapie are not fundamentally involved in the development of disease but represent mainly secondary changes.

Animals↗