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P Carthew

Publications and source records attributed to P Carthew.

84 records · Page 5Linked to original sources
PubMed1978

Peroxidase-labeled antibody technique for rapid detection of mouse hepatitis virus in cases of natural outbreaks.

A recent outbreak of hepatitis in mice at the Laboratory Animals Centre (Surrey, England) is described. The only strains of mice that showed clinical symptoms and typical liver lesions were the nude (nu/nu) and obese mice. Although other inbred strains showed no clinical symptoms, all strains seroconverted. Neutralization typing of the mouse hepatitis virus showed it to be type 1, a hepatotropic strain of low virulence, a finding that was consistent with the pathology of the disease. Because of recurring outbreaks of disease caused by this strain and other strains of MHV in the United Kingdom, a rapid method for diagnosis in tissue culture was devised, employing the peroxidase enzyme-labeled antibody technique for detection of mouse hepatitis virus in L-929 cells.

Animals↗
PubMed1978

A serological survey of accredited breeding colonies in the United Kingdom for common rodent viruses.

This paper reports the results of a general survey, the first in the United Kingdom, carried out on accredited breeding colonies of mice, rats and guinea-pigs over a period of a year. While the results show the potential usefulness of a viral accreditation grading scheme, they also show that contamination of breeding colonies with inapparent viral infections is widespread. This situation can only be improved by the continuous monitoring of animal stocks for rodent viruses, with the aim of improving the standard of animals available for research and for pharmacological, toxicological and routine diagnostic procedures.

Animals↗
PubMed1976

The surface nature of proteins of a bovine enterovirus, before and after neutralization.

The surface nature of the proteins of a bovine enterovirus have been determined by using 125I and pyridoxal phosphate-sodium borohydride labelling techniques. As found previously, 125I labels only VP1 in intact capsid particles, whereas reaction with pyridoxal phosphate followed by reduction with tritiated sodium borohydride labels VP1, VP2 and VP3. Only VP4 is found to have no surface tyrosine, histidine or lysine available for reaction. After neutralization with homologous antisera, however, VP4 becomes exposed and is then available for labelling with 125I. This must reflect a substantial conformational change in the virus particle after neutralization.

Animals↗
PubMedDate not supplied

Method for determining whether the number of hepatocytes in rat liver is increased after treatment with the peroxisome proliferator gemfibrozil.

A histological method has been developed for determining the absolute numbers of rodent hepatocytes after treatment with the hypolipodemic drug gemfibrozil. It can be applied to distinguish between the enlargement of the liver that commonly occurs in rodents after treatment with chemicals, due to changes in the size of cells (hypertrophy), rather than an increase in the number of cells caused by cell division (hyperplasia). In the case of gemfibrozil the liver enlargement was found to be partly due to hypertrophy and partly to hyperplasia. The induction of hyperplasia can be associated with an increased risk of eventual liver tumour formation, and the distinction of hypertrophy from hyperplasia using a purely histological method, for the determination of increases in hepatocyte cell numbers, will be useful in the assessment of compounds which cause liver enlargement that could precede neoplasia.

Animals↗
PubMedDate not supplied

Pathological mechanisms of hepatic tumour formation in rats exposed chronically to dietary hexachlorobenzene.

The chronic dietary administration of hexachlorobenzene (HCB) to rats for a year or more results in the formation of liver tumours described as hepatocellular carcinomas, hepatomas or haemangiomas. The hepatotoxicity of HCB, which is greatest in hamsters and rats, gives rise to peliosis and necrosis with haemosiderosis. This pattern of hepatotoxicity indicates vascular damage, which through haemosiderosis could increase not only the toxic effect of HCB to hepatocytes but also its tumourogenic potential. The present study confirmed vascular damage by the identification of widespread fibrin deposits in the livers of rats chronically exposed to HCB, using an antibody to rat fibrin. Based on our study we suggest that the formation of hepatomas and haemangiomas with elements of peliosis (cystic blood-filled cavities) could be explained by the compensatory hyperplastic responses to hepatocellular necrosis and by the simultaneous loss of hepatocellular cords. The accumulation of iron in the liver would strongly potentiate the development of hepatic tumours, as has been found in HCB and polychlorinated biphenyl-treated mice with iron overload. The implications of this non-genotoxic mechanism of hepatoma formation for the assessment of human health risk are discussed.

Administration, Oral↗