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Biomedical subjects

B J Sheahan

Publications and source records attributed to B J Sheahan.

At least 55 records · Page 3Linked to original sources
PubMed1986

Ageing changes in the bovine kidney.

A study of macroscopically normal bovine kidneys from three age groups (neonatal calves, 2.5- to 3-year-old bullocks and cull cows), with no abnormalities on urine analysis, was carried out by light microscopy, immunofluorescence and electron microscopy. There was a slight increase in the proportion of involuted nephrons with increasing age but the proportion of nephrons affected was not greater than 10 per cent in any age group. In contrast to the findings of earlier workers, no evidence of diffuse proliferative glomerulonephritis was found in the material examined. It was concluded that the above techniques should be applied to the investigation of renal disease in cattle, as has already been done in man and small domestic animals.

Aging↗
PubMed1985

The pathogenicity of the A7, M9 and L10 strains of Semliki Forest virus for weanling mice and primary mouse brain cell cultures.

The multiplication of the M9, A7 and L10 strains of Semliki Forest virus (SFV), both in weanling mice and primary mouse brain cell cultures, was compared. Following both intraperitoneal (i.p.) and intracerebral (i.c.) injection, the virulent L10 strain multiplied to higher titre in the mouse central nervous system (CNS) than did the less virulent M9 and A7 strains, whereas M9 multiplied to higher titre than A7. By the i.c. route, all three virus strains multiplied to higher titre than following i.p. injection. Multiplication of A7 and M9 in oligodendrocytes, but not neurons, was detected following i.c. injection. All three virus strains showed a tropism for cultured mouse glial cells rather than neurons. The L10 strain multiplied better in neurons than did A7 or M9. It is concluded that the mechanism of acute demyelination induced by the M9 and A7 strains is similar. Based on this and previous studies, it is proposed that infection of glial cells triggers immune-mediated demyelination. The virulence of the L10 strain is due to its ability to exceed a lethal threshold of damage to neurons before immune intervention can occur.

Animals↗
PubMed1984

The pathogenicity of the M9 mutant of Semliki Forest virus in immune-compromised mice.

The role of immune mechanisms in the pathogenicity of the M9 mutant of Semliki Forest virus (SFV) has been examined by the use of immune-deficient and immune-suppressed mice. In immune-competent BALB/c and C57BL/6 mice, the lesions in the central nervous system (CNS) were characterized by acute demyelinating meningoencephalomyelitis. Myelin vacuolation and demyelination were more severe in BALB/c mice than in mice with a C57BL background. The mortality was 12% and 29% respectively. Treatment with cyclophosphamide or sodium aurothiomalate did not greatly alter the type of lesion produced, although mortality was increased. Lesions were less severe in nude (T-lymphocyte-deficient) mice and more severe in beige (natural killer cell-deficient) mice than in most immune-competent mice. Mortality was marginally increased in nude mice but not in beige mice. Demyelination in nude mice was followed rapidly by remyelination. Immune modification did not significantly alter the titres of virus in the brain at 7 days post-infection and infectious virus had been cleared from the brain by 14 days in all cases. Degenerating oligodendrocytes were detected in the CNS of all immune-modified mice examined at day 7. This study therefore suggests that both immune mechanisms and destruction of oligodendrocytes play a role in the production of demyelination by M9.

Animals↗
PubMed1984

Hepatic infarction with absolute ethanol.

Ethanol was used to embolize the hepatic artery in 7 dogs, producing occlusion proportional to the dose employed. On follow-up angiography at 1 and 4 weeks, occlusion was unchanged or more pronounced, indicating that such embolization is permanent. Because ethanol is nonviscous and easy to use, it is effective in occluding the hepatic arterial system. Perisinusoidal fibrosis is produced.

Animals↗
PubMed1983

Oligodendrocyte infection and demyelination produced in mice by the M9 mutant of Semliki Forest virus.

Intraperitoneal inoculation with the M9 mutant of Semliki Forest virus caused focal demyelinating encephalomyelitis in weanling BALB/c and C57BL/6 mice. Demyelination was more severe in BALB/c than in C57BL/6 mice. Virus particles were seen in oligodendrocytes in areas of myelin vacuolation 5 and 7 days post inoculation (DPI). Oligodendrocytes containing virus in BALB/c mice showed hypertrophy and vacuolar degeneration. There was a mononuclear cell infiltrate and lymphocytes and necrotic cells were present in vacuoles in myelin sheaths. Demyelinating plaques containing macrophages laden with myelin debris were most prominent 14 DPI when virus was cleared from the brain. Remyelination of the central type occurred 28 DPI in BALB/c mice. These findings indicate that direct virus-induced injury to oligodendrocytes has a major role in the initiation of inflammation and demyelination in this model system.

Animals↗
PubMed1982

Semliki forest virus neurovirulence mutants have altered cytopathogenicity for central nervous system cells.

We have analyzed the pathogenicity and host range properties of four neurovirulence mutants of Semliki Forest virus which, unlike the wild type (WT), allow the survival of weanling mice injected intraperitoneally with 10(2) PFU. The mutant M9 showed a sustained multiplication in the brains of infected mice. It produced paralysis in 35%, and 8% died. Demyelination occurred in 94% of the surviving mice and was associated with the destruction of oligodendrocytes. All of the mutants showed a restricted ability to multiply in BHK, C1300 (neuroblastoma), and G26-24 (oligodendroglioma) cells as compared with the WT, and this was not associated with differential interferon production or action. C1300 cells infected with the mutants survived, whereas WT-infected cells were killed. In G26-24 cells all of the mutants and the WT produced a rapid cytopathic effect which was inhibited by pretreatment with 10 U of mouse interferon. Extensive RNA synthesis was detected for all of the mutants and the WT in BHK and C1300 cells, but it was only detectable in G26-24 cells in small amounts early in the infection. The mutant M4 had a defect in the nucleocapsid assembly, whereas M9 had a defect in total RNA synthesis. M136 was defective in the synthesis of 26S RNA, and M103 showed defective synthesis of viral core protein in C1300 cells. It is concluded that C1300 cells can tolerate viral RNA synthesis by a defective virus without showing a cytopathic effect, but the fully virulent WT virus is cytopathic. G26-24 cells are sensitive to small amounts of viral RNA synthesis. These properties of the WT and mutant viruses correlate with changes produced in the neurons and oligodendrocytes of the central nervous system: the virulence of the WT is due to its ability to destroy both neurons and oligodendrocytes, whereas the demyelination produced by the mutants M9 and M136 is due to the destruction of oligodendrocytes alone.

Animals↗
PubMed1982

Effect of alphavirus infection on mouse embryos.

Seven strains and mutants of the alphaviruses, Semliki Forest virus and Sindbis virus, differed in their lethality for mouse embryos and their mothers. The A7 strain and the neurovirulence mutant M103 of Semliki Forest virus were selected for detailed comparison. A7 produced 100% lethality of mouse embryos but was avirulent for their mothers. M103 did not kill embryos or their mothers but did induce postnatal immunity. This immunity could be induced in utero or by suckling to an immune mother. Infectious virus could be recovered from the brain, blood, and embryos of mice infected with A7. Mice infected with M103 developed a viremia of similar titer, but virus could not be recovered from brain or embryos. Electron microscopy showed multiplying virus in trophoblast and fetal tissue after infection with A7, but no virus could be detected in such tissue after infection with M103. Cultures of ectoplacental cone trophoblast cells incubated in the presence of A7 or M103 showed multiplying A7 in the giant cells, but no M103. It is concluded that A7 can traverse both the blood-brain barrier and the placenta, whereas M103 can traverse neither.

Animals↗
PubMed1981

Demyelination in mice resulting from infection with a mutant of Semliki Forest virus.

Twelve of 34 weanling mice (35%) developed lesions in the brain and spinal cord following i.p. infection with 10(2) p.f.u. of a mutant of Semliki Forest virus (SFV). Six of 12 mice examined 13 days post infection (p.i.) showed meningo-encephalomyelitis with focal spongiform lesions in the grey and white matter. The spongiform lesions were characterised by necrosis of putative oligodendrocytes, myelinic vacuolation and mononuclear cell infiltration. Only one of six mice examined 21 days p.i. and one of six mice examined 28 days p.i. showed lesions which comprised reactive and dystrophic changes in the white matter. Spongiform lesions and pycnotic nuclei were not seen at these times. Viral nucleocapsids were seen in the early stages of the disease in putative necrotic oligodendrocytes. Mature virus particles were not seen. This was in contrast to mice infected with virulent wild-type SFV when lesions were more severe and were accompanied by large numbers of immature and mature virus particles. It is suggested that the demyelination in mice infected with mutant SFV results primarily from selective destruction of oligodendrocytes by the mutant virus.

Animals↗
PubMed1980

Isolation and preliminary characterization of Semliki Forest virus mutants with altered virulence.

Four mutants of Semliki Forest virus (SFV) strain Lio showing altered virulence in weanling mice were selected following mutagenesis with N-nitro-N-methyl-N'-nitrosoguanidine. Intraperitoneal (i.p.) injection of wild-type (wt) virus resulted in the death of all mice given more than 30 p.f.u. Protection of mice surviving injection with lower doses of virus was not obtained. A proportion of mice infected with doses from 10(4) to 10(7) p.f.u. of mutant virus survived infection. Such surviving mice were protected against an otherwise lethal challenge with wt virus. Three mutants which were non-lethal at loses of 10(2) p.f.u. were studied further. The mutants M4 and M103 established a transient viraemia which was quickly cleared; unlike the wild-type, the virus did not enter the brain or spinal cord. The mutant M136 produced a viraemia similar to the wild-type, but reached a lower titre in the brain; it was not recovered from the spinal cord. Severe necrotic and inflammatory lesions, associated with large numbers of virus particles, were present in the brain and spinal cord (CNS) of mice 5 days p.i. with wt virus. Mice infected with M136 showed degenerative lesions in the grey and white matter of the CNS at 13 days p.i. Virus particles could not be detected at this time either by electron microscopy or infectivity assays.

Animals↗
PubMed1980

Histiolymphocytic lymphosarcoma in the subcutis of two horses.

Two aged mares with histiolymphocytic lymphosarcoma had multiple rapidly proliferating tumours in the subcutis. Consistent haematological changes were absent. One mare had lymph node involvement but no neoplastic lesions in the viscera. Microbiological examination of tumour tissue showed coryneform bacteria; there was no evidence of C-type or lytic viruses or of reverse transcriptase. Prominent intramitochondrial crystalline inclusions were in histiocytic tumour cells.

Animals↗
PubMed1978

Ocular pathology of bovine GM1 gangliosidosis.

Late-onset of disturbed vision is a clinical feature of bovine GM1 gangliosidosis. Studies on eight affected calves showed that ocular lesions were confined to the retinae and optic nerves. Myriad tiny white spots were visible by ophthalmic examination of the fundus. These spots were related to protuberances on the vitreal surface caused by distended retinal ganglion cells. The perikaryons of these were packed with dense aggregates of membranous cytoplasmic bodies (MCBs). Similar MCBs were present in the perikaryons of amacrine cells in the inner nuclear layer of the retina. Wallerian degeneration was present in the optic nerves. The lesions were compared with those described in gangliosidosis in man, cats, pigs and dogs. It is suggested that examination of the fundus is a useful clinical procedure in the diagnosis of bovine GM1 gangliosidosis.

Animals↗
PubMed1977

The glycosaminoglycan content of the liver in bovine GM1 gangliosidosis.

Chemical analysis of the livers from four calves with GM1 gangliosidosis was negative for significantly elevated levels of glycosaminoglycans. The chemical findings confirmed morphological studies in which hepatic changes were minimal or absent. The findings were compared with the published evidence for the hepatic storage of glycosaminoglycans in human GM1 gangliosidosis.

Animals↗