Genetic analysis of the naked trait in panicles of hexaploid oat

The aim of this study was to estimate the number of genes that control the naked (hull-less) trait and the mode of expression of this characteristic in panicles of hexaploid white oat. Parents and the segregating population (in the F2 and F3 generations) were evaluated in regard to the presence and distribution of naked grains in panicles of individual oat plants. For each plant, a drawing of the main panicle was developed. From the drawings obtained in the progenies of the F2 population, six distinct phenotypic classes were produced. The expected phenotypic proportion of 3:9:4 (naked:segregating:hulled) was that which best fit by the Chi-square test. In the F3 generation, the results showed agreement with the hypothesis observed in the F2 generation. The naked trait in oat is passed on by two genes and the greatest expression of this trait occurs in the upper third of the panicles. Expression of this trait in oats is not complete, even in homozygous genotypes

Induction of eosinophil apoptosis by hydrogen peroxide promotes the resolution of allergic inflammation

Made available in DSpace on 2015-08-19T13:49:23Z (GMT). No. of bitstreams: 2 license.txt: 1914 bytes, checksum: 7d48279ffeed55da8dfe2f8e81f3b81f (MD5) ma_martins_etal_IOC-2105.pdf: 3830001 bytes, checksum: 2629ef32ff4c6dfb811625d5ef43b612 (MD5) Previous issue date: 2015Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Morfologia. Laboratório de Resolução da Resposta Inflamatória. Laboratório de Imunofarmacologia. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brasil.University of Edinburgh. The Queen’s Medical Research Institute. Medical Research Council Centre for Inflammation Research. Edinburgh, Scotland, UK.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Morfologia. Laboratório de Resolução da Resposta Inflamatória. Laboratório de Imunofarmacologia. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brasil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Morfologia. Laboratório de Resolução da Resposta Inflamatória. Laboratório de Imunofarmacologia. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brasil.Universidade Federal de Minas Gerais. Faculdade de Farmácia. Departamento de Análises Clínicas e Toxicológicas. Laboratório de Sinalização na Inflamação. Belo Horizonte, MG, Brasil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Microbiologia. Belo Horizonte, MG, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Inflamação. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Inflamação. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Inflamação. Rio de Janeiro, RJ, Brasil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Laboratório de Patologia Geral. Belo Horizonte, MG, Brasil.Universidade Federal de Minas Gerais. Faculdade de Farmácia. Departamento de Análises Clínicas e Toxicológicas. Laboratório de Sinalização na Inflamação. Belo Horizonte, MG, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Inflamação. Rio de Janeiro, RJ, Brasil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Morfologia. Laboratório de Resolução da Resposta Inflamatória. Belo Horizonte, MG, Brasil.University of Edinburgh. The Queen’s Medical Research Institute. Medical Research Council Centre for Inflammation Research. Edinburgh, Scotland, UK.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Laboratório de Imunofarmacologia. Belo Horizonte, MG, Brasil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Morfologia. Laboratório de Resolução da Resposta Inflamatória. Laboratório de Imunofarmacologia. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brasil.Eosinophils are effector cells that have an important role in the pathogenesis of allergic disease. Defective removal of these cells likely leads to chronic inflammatory diseases such as asthma. Thus, there is great interest in understanding the mechanisms responsible for the elimination of eosinophils from inflammatory sites. Previous studies have demonstrated a role for certain mediators and molecular pathways responsible for the survival and death of leukocytes at sites of inflammation. Reactive oxygen species have been described as proinflammatory mediators but their role in the resolution phase of inflammation is poorly understood. The aim of this study was to investigate the effect of reactive oxygen species in the resolution of allergic inflammatory responses. An eosinophilic cell line (Eol-1) was treated with hydrogen peroxide and apoptosis was measured. Allergic inflammation was induced in ovalbumin sensitized and challenged mouse models and reactive oxygen species were administered at the peak of inflammatory cell infiltrate. Inflammatory cell numbers, cytokine and chemokine levels, mucus production, inflammatory cell apoptosis and peribronchiolar matrix deposition was quantified in the lungs. Resistance and elastance were measured at baseline and after aerosolized methacholine. Hydrogen peroxide accelerates resolution of airway inflammation by induction of caspase-dependent apoptosis of eosinophils and decrease remodeling, mucus deposition, inflammatory cytokine production and airway hyperreactivity. Moreover, the inhibition of reactive oxygen species production by apocynin or in gp91phox −/− mice prolonged the inflammatory response. Hydrogen peroxide induces Eol-1 apoptosis in vitro and enhances the resolution of inflammation and improves lung function in vivo by inducing caspase-dependent apoptosis of eosinophils