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Biomedical subjects

C E Piper

Publications and source records attributed to C E Piper.

29 records · Page 2Linked to original sources
PubMed1978

Natural mode of transmission of the bovine leukemia virus: role of bloodsucking insects.

The development of bovine leukemia virus (BLV) infection was studied in 14 noninfected young adult cattle exposed to 25 to 30 BLV-infected cows in an area of approximately 0.5 ha. Of 7 cattle (group 1) exposed beginning in July and August (midsummer) of 1976, 4 were infected by October, and all 7 by November (4 months' exposure). Of 7 cattle (group 2) exposed from February 1977 (midwinter), all remained negative for 3 months, and only 1 was positive after 6 months. By October 1977, however, 4 cattle in this group were infected, indicating that contact transmission of BLV is prevalent during the summer months. This, and the fact that BLV-infected lymphocytes were recovered from tabanids allowed to feed on a BLV-positive cow, supports the idea that bloodsucking insects play a major role in the spread of BLV.

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PubMed1978

An evaluation of the role of milk in the natural transmission of BLV.

In order to evaluate the role of milk in the transmission of BLV, the presence of the virus and viral antibodies was investigated in cattle that were born to, and nursed on, infected dams and then raised in isolation or in contact with infected animals. Only 3 of the 17 isolated cattle became infected during 25-29 months of observation. During the same period of time, all 17 cattle raised in contact with BLV-positive animals developed BLV infection. From these results, it is apparent that milk-borne transmission of BLV, if it occurs, is much less frequent than contact transmission.

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PubMed1977

Cellular basis of persistent lymphocytosis in cattle infected with bovine leukemia virus.

Peripheral blood lymphocytes from 14 cattle infected with the bovine leukemia virus (BLV) and 14 BLV-free cattle were examined by the membrane immunofluorescent antibody technique to detect surface immunoglobulin (S-Ig) and by the erythrocyte-antibody-complement (EAC) rosette test for the detection of complement receptors. Direct comparisons of the percentages of S-Ig-bearing cells and EAC rosette-forming cells in both infected and BLV-free animals showed no evidence for the presence of a substantial population bearing one surface marker but not the other. The data showed that cells with surface markers characteristic of B lymphocytes are responsible for most of the increase in peripheral blood lymphocytes which may accompany BLV infection. The release of infectious BLV and the spontaneous uptake of thymidine by short-term cultured peripheral blood lymphocytes from BLV-infected cattle were also studied. The results indicate that both of these activities are function of B lymphocytes.

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PubMed1977

Properties of density gradient-fractionated peripheral blood leukocytes from cattle infected with bovine leukemia virus.

Discontinuous bovine serum albumin gradients were used to fractionate peripheral blood leukocytes from bovine leukemia virus (BLV)-free and BLV-infected cows. The release of infectious BLV and spontaneous incorporation of [3H]thymidine were not properties of density gradient-fractionated leukocytes from a BLV-free cow. When leukocytes from BLV-infected cattle were fractionated, B lymphocytes which spontaneously incorporated [3H]thymidine could be separated as a distinct subpopulation from B lymphocytes which replicated infectious BLV. Density gradient fractionation of leukocytes from a cow with lymphosarcoma is also reported. A fall in lymphocyte count at the time of tumor development is attributed to the loss of B lymphocytes which spontaneously incorporate [3H]thymidine.

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PubMed1975

Seroepidemiological evidence for horizontal transmission of bovine C-type virus.

Thirty colostrum-deprived calves from leukemia-free herds were foster nursed for 10 weeks on cows infected with bovine C-type virus (BLV) from multiple-case herds or on cows from leukemia-free herds. After weaning, the calves were raised in continuous contact with BLV-infected animals of approximately the same ages. Sera collected at 6 to 18 and 43 to 48 months of age were examined for the presence of antibodies to BLV by the immunofluorescent antibody test. At 6 to 18 months of age, only 1 of the 30 calves from leukemia-free herds had a detectable antibody response to BLV. By 43 to 48 months of age the number of antibody-positive animals had risen to 17. The foster dam's herd of origin did not significantly affect the rate of BLV infection. These results indicate that BLV can be horizontally transmitted from infected to noninfected animals.

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PubMedDate not supplied

Genetic toxicology studies with a tumor promoter.

A diuretic antihypertensive agent, SC-33643 (8-[2-ethoxyethyl]-7-phenyl-[1,2,4]triazolo[4,3-c]pyrimidine-5- amine, also known as bemitradine), was tested in the Ames test, in the mouse lymphoma TK +/- mutation assay, in the Chinese hamster ovary cell hypoxanthine guanine phosphoribosyl transferase (CHO/HGPRT) mutation test and in the CHO chromosome aberration assay with and without metabolic activation. Additionally, the compound was tested in the rat primary hepatocyte unscheduled DNA synthesis (UDS) assay and in the mouse bone marrow micronucleus assay. The results were uniformly negative. Contrary to expectations based on the results of the battery of genetic toxicology tests, the compound produced liver, thyroid and mammary tumors in the rat (reported separately). Subsequently, SC-36741 (5-amino-7-phenyl-[1,2,4]triazolo-[1,5-c] pyrimidine-8-ethanol, also known as desethylbemitradine), a major metabolite of SC-33643, was tested in the Ames test, in the CHO/HGPRT mutation test and in the CHO chromosome aberration assay with and without metabolic activation, and was also tested in the rat primary hepatocyte/UDS assay and in the mouse bone marrow micronucleus assay. This metabolite also produced negative results in these tests. Therefore, SC-33643 is a non-genotoxic carcinogen producing tumors in rats without altering DNA or chromosomes.

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PubMedDate not supplied

Mutagenicity of chloropropanol in a genetic screening battery.

A 72:25 mixture of 1-chloro-2-propanol and 2-chloro-1-propanol was tested for genetic activity in a battery of short term tests. Chloropropanol was tested over a dose range of 527-167,250 micrograms/plate in the Salmonella/mammalian microsome mutagenicity assay. A dose dependent mutagenic response was observed in strains TA 1535 and TA 100. Metabolic activation enhanced mutagenicity in both strains. Although chloropropanol was mutagenic in the TK+/-mouse lymphoma assay with and without metabolic activation, a smooth linear dose response relationship was not observed. Non-toxic mutagenic doses ranged from 5,000 to 10,000 micrograms/mL without activation. Chloropropanol was also mutagenic in the rat bone marrow cytogenetic assay. Rats dosed orally with 10, 31 and 100 mg/kg/day for 5 days displayed no significant difference in mean body weight gain or mean mitotic index when compared to controls, however, a dose-response increase (significant) in the number of aberrations, mostly chromatid breaks, was observed in each case.

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PubMedDate not supplied

A critical appraisal of the value of the mouse cancer bioassay in safety assessment.

Substantial progress in understanding nongenotoxic or secondary mechanisms of tumorigenesis has been made over the past decade. However, the methods used in regulated studies for assessment of carcinogenic potential in chemicals in development have not evolved significantly. Based on the experience of over 30 yr of testing and the societal need to control costs, reevaluation of standard cancer rodent bioassay protocols is being done. Expert consensus after evaluating the results of full-scale rodent bioassays of both sexes in 2 species is that a reduced protocol is acceptable. After review of relevant data, it is our opinion that cancer hazard assessment in male and female rats only would be sufficient and that, in the future, mouse bioassays will not add significant value on a routine basis. We are unable to find an example of a mouse tumorigenic finding that predicts a confirmed or probable human response with negative findings in a rat bioassay. The savings realized by eliminating mouse testing from routine protocols would be substantial and better spent in expanding short-term studies to add to our understanding of chemical carcinogenesis.

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