ResearchPad - investigations-on-nonhuman-systems https://www.researchpad.co Default RSS Feed en-us © 2020 Newgen KnowledgeWorks <![CDATA[Differential Distribution of Mouse Mammary Tumor Virus-Related Sequences in the DNA’s of Rats<a href="#FN1"><sup>2</sup></a>]]> https://www.researchpad.co/article/elastic_article_11649 Radioactively labeled mouse mammary tumor virus (MuMTV) 60-70S RNA, obtained from virions grown In both murine and feline cells, was employed In molecular hybridization experiments to detect MuMTV-related sequences In the DNA’s of rats (Rattus norveglcus). With the use of relaxed conditions of hybridization and assay for RNA-DNA duplexes, all strains of laboratory rats and feral rats examined were shown to possess endogenous MuMTV-related DNA sequences In the low repetitive range. These sequences were related to approximately 20% of the MuMTV genome and exhibited a melting temperature (Tm) approximately 5° C lower than MuMTV-specific proviral sequences In murine (Mus musculus) DNA’s. Certain colonies of the F344 strain of rat (Fischer) contained animals whose DNA’s possessed additional MuMTV-related sequences. These sequences were related to the non-germ-line-transmitted, tumorassociated (TA) sequences of the highly oncogenic MuMTV (C3H). They were found In the DNA of some F344 rats and a cloned established F344 rat embryo cell line at a frequency of approximately one copy per haploid genome and exhibited a Tm 9° C lower than that of hybrid duplexes formed between radioactive MuMTV TA-sequence RNA and C3H mouse mammary tumor DNA. The DNA’s of rats, therefore, contained two sets of sequences that were related to sequences of the MuMTV genome: One set was germ-line transmitted, whereas the other set appeared to be transmitted in some rats via a non-germ line or infectious process.

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<![CDATA[Determinants of Susceptibility and Resistance to Feline Leukemia Virus Infection. I. Role of Macrophages<a href="#FN2"><sup>2</sup></a><a href="#FN3"><sup>3</sup></a>]]> https://www.researchpad.co/article/elastic_article_11647 The role of autochthonous peritoneal feline macrophages (Mθ) in the age-related resistance of cats to feline leukemia virus (FeLV) was investigated by a study of the functional properties and FeLV susceptibility of Mθ from kittens and adult cats and the effect of hydrocortisone (HC) and silica on Mθ-FeLV interactions. Although the phagocytic functions of isolated Mθ from kittens and adults were equivalent, the mean FeLV susceptibility of Mθ from kittens was five times that of Mθ from adult cats, thus establishing a direct correlation between the age-related susceptibility of cats and Mθ from cats to FeLV. Mθ of viremic cats were found to be infected with FeLV in vivo; virus titers were slightly higher than those obtained after in vitro infection of Mθ. Mθ from cats that had experienced regressive FeLV infection were not significantly more resistant to FeLV infection in vitro than were Mθ from naive adult specific-pathogen-free cats. HC, which has been shown to enhance the in vivo FeLV susceptibility of cats, also enhanced the permissiveness of Mθ from cats to FeLV in vitro (600-fold for Mθ from adult cats and 200-fold for Mθ) from kittens. Mθ permissiveness to FeLV was highly sensitive to HC and occurred in Mθ infected in vivo or in vitro. In parallel with the effect of HC on the natural resistance of cats to FeLV, administration of silica before virus inoculation also markedly enhanced the FeLV susceptibility of adult cats. Silica was toxic for isolated Mθ but not for lymphocytes in vitro, and silica produced monocytopenia and neutrophilia, delayed skin allograft rejection, and augmented feline oncovirus-associated cell membrane antigen antibody responses in vivo. These experiments indicate that Mθ were linked to the natural resistance of cats to FeLV and that the temporary elimination of Mθ functions (e.g., by silica) and/or the conversion of the Mθ-FeLV relationship from a nonpermissive to a permissive state (e.g., by corticosteroids) resulted in failure of early virus containment, in persistent virus amplification in hemolymphatic tissues, and in subsequent FeLV-related proliferative or antiproliferative disease.

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<![CDATA[Pathogenesis of Lesions Induced in Rat Lung by Chronic Tobacco Smoke Inhalation<a href="#FN2"><sup>2</sup></a><a href="#FN3"><sup>3</sup></a>]]> https://www.researchpad.co/article/elastic_article_11644 Lesions were induced in the lungs of specific-pathogen-free F344 rats by chronic tobacco smoke exposure. Animals exposed to 7 cigarettes/day were killed after 1, 1.5, or 2 years of exposure. Parallel lifetime exposures induced pulmonary tumors in 9% of the animals. In serially killed animals, four types of lesions were found: 1) perivascular or peribronchiolar accumulation of lymphoreticular cells, 2) fibrotic and cellular enlargement of peribronchiolar septa, 3) type II cell hyperplasia with septal fibrosis, and 4) air-space enlargement (emphysema). However, emphysema occurred only in animals exposed to a higher (10 cigarettes) dose of tobacco smoke. Ultrastructural studies showed all of the focal lesions to be infiltrated by cells typical of the inflammatory response. The type II hyperplastic and peribronchiolar alveolar lesions involved larger portions of the parenchyma in fibrotic changes but differed in structure, location, and frequency. The incidence of the peribronchiolar alveolar lesions was temporally related to tumor incidence.

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