Ectromelia
Mostrando 1-12 de 44 artigos, teses e dissertações.
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1. Bilateral tibial hemimelia tipo 1 (1a e 1b) com hemivertebras T9 e T10: uma nova associacao
CONTEXTO Ausência congênita da tíbia é uma anomalia rara, com incidência em 1 por 1.000.000 de nascidos vivos, é principalmente esporádica e pode ser identificada como um distúrbio isolado ou como parte de síndromes de malformações. RELATO DO CASO Criança do sexo masculino, nascida de pais não afetados e não consanguíneos, apresentou-se com
Sao Paulo Med. J.. Publicado em: 2013
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2. Evaluation of an enzyme-linked immunosorbent assay for the detection of ectromelia (mousepox) antibody.
Ectromelia virus, an orthopoxvirus that can cause extensive morbidity and mortality (mousepox) in colonized mice, has been epizootically responsible for serious disruption of biomedical research since 1930. The lack of a sensitive and specific serological assay for infection with this virus became apparent during outbreaks of mousepox at the National Institu
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3. Combined protective effects on interferon and interferon induction on herpes simplex and ectromelia virus infections in mice.
Mouse interferon or the induction of mouse interferon with polyriboinosinic acid-polyribocytidylic acid significantly protected mice against herpes simplex and ectromelia viral infections. When polyriboinosinic acid-polyribocytidylic acid was administered 24 h before herpes simplex or ectromelia viral infection and mouse interferon was administered shortly b
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4. Genetic Variability of Immunomodulatory Genes in Ectromelia Virus Isolates Detected by Denaturing High-Performance Liquid Chromatography
The genetic variability of nine genes in 12 isolates and strains of ectromelia virus, which causes a smallpox-like disease (mousepox) in mice, was determined and allows for classification of ectromelia viruses. The low genetic variability suggests that evolutionary pressure maintains the activity of immunomodulatory genes in natural poxvirus infections.
American Society for Microbiology.
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5. Abrogation of resistance to severe mousepox in C57BL/6 mice infected with LP-BM5 murine leukemia viruses.
Strain C57BL/6 (B6) mice infected with LP-BM5 murine leukemia virus (MuLV) develop a disease which combines abnormal lymphoproliferation with profound immunosuppression and has many features in common with human acquired immunodeficiency syndrome induced by HTLV-III/LAV retroviruses. To determine whether this LP-BM5 MuLV infection would affect the innate res
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6. Effect of Mycobacterium tuberculosis BCG infection on the resistance of mice to ectromelia virus infection: participation of interferon in enhanced resistance.
Mice infected with Mycobacterium tuberculosis BCG were more resistant than normal mice to ectromelia virus infection. It is suggested that enhanced interferon production in peritoneal exudate cells and spleen cells of BCG-infected mice plays an important role in this resistance.
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7. Mechanisms of enhanced resistance of Mycobacterium bovis BCG-treated mice to ectromelia virus infection.
The mechanism of enhanced resistance of Mycobacterium bovis BCG-treated mice to ectromelia virus infection was investigated by determining the effect of splenectomy, antithymocyte serum, and antimacrophage serum on resistance. It was greatly reduced by these treatments, not only in normal mice, but also in mice treated with live or heat-inactivated BCG. Prod
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8. Mechanisms determining innate resistance to ectromelia virus infection in C57BL mice.
The mechanism for innate resistance to ectromelia virus, which is controlled by a single gene in C57BL mice, was investigated. The cells or factors involved appear to be radioresistant and to impose an early barrier to viral penetration and spread via lymphatics or blood to the target organs, i.e., liver and spleen.
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9. Role of Hemopoietic Colony-Forming Cell Responses in the Pathogenesis of Ectromelia
Intraperitoneal injection of complete Freund's adjuvant which caused an extensive cellular response in the reticuloendothelial system greatly increased the severity of infection which resulted from footpad inoculation of ectromelia virus in mice. The mortality was greatest during the proliferative phase of the cellular response, indicated by the colony-formi
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10. Chromosomal locations and gonadal dependence of genes that mediate resistance to ectromelia (mousepox) virus-induced mortality.
Four genetic loci were tested for linkage with loci that control genetic resistance to lethal ectromelia virus infection in mice. Three of the loci were selected because of concordance with genotypes assigned to recombinant inbred (RI) strains of mice derived from resistant C57BL/6 and susceptible DBA/2 (BXD) mice on the basis of their responses to challenge
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11. Effect of Cell Dose and Dose of Infectious Agent on Expression of Protection Against Listeria monocytogenes and Ectromelia Virus in Cell Transfer Models
Two parameters (immune cell dose and dose of infectious agent) influencing the expression of protection by transferred immune spleen cells in Listeria monocytogenes and ectromelia virus infection in mice were investigated. First, when recipient mice were infected with a constant dose of ectromelia virus, a linear relationship between log10 cells transferred
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12. Role of specific cytotoxic lymphocytes in cellular immunity against murine cytomegalovirus.
Cytotoxic lymphocytes were generated in vitro against murine cytomegalovirus (MCMV)-infected cells by incubation with ultraviolet light-irradiated, infected fibroblasts. When passively transferred, they reduced virus titers in spleens of mice 1 day after infection with MCMV. Protection was abrogated by anti-theta serum and complement. Spleen cells from mice