16 research outputs found
Three-Dimensional Magnetic Reconnection
The importance of magnetic reconnection as an energy release mechanism in
many solar, stellar, magnetospheric and astrophysical phenomena has long been
recognised. Reconnection is the only mechanism by which magnetic fields can
globally restructure, enabling them to access a lower energy state. Over the
past decade, there have been some major advances in our understanding of
three-dimensional reconnection. In particular, the key characteristics of 3D
magnetohydrodynamic (MHD) reconnection have been determined. For instance, 3D
reconnection (i) occurs with or without nulls, (ii) occurs continuously and
continually throughout a diffusion region and (iii) is driven by counter
rotating flows.
Furthermore, analysis of resistive 3D MHD magnetic experiments have revealed
some intriguing effects relating to where and how reconnection occurs. To
illustrate these new features, a series of constant-resistivity experiments,
involving the interaction of two opposite-polarity magnetic sources in an
overlying field, are considered. Such a simple interaction represents a typical
building block of the Sun's magnetic atmosphere. By following the evolution of
the magnetic topology, we are able to explain where, how and at what rate the
reconnection occurs. Remarkably there can be up to five energy release sites at
anyone time (compared to one in the potential case) and the duration of the
interaction increases (more than doubles) as the resistivity decreases (by a
factor of 16). The decreased resistivity also leads to a higher peak ohmic
dissipation and more energy being released in total, as a result of a greater
injection of Poynting flux.Comment: To appear in "Magnetic Coupling between the Interior and the
Atmosphere of the Sun", eds. S.S. Hasan and R.J. Rutten, Astrophysics and
Space Science Proceedings, Springer-Verlag, Heidelberg, Berlin, 200
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
Plankton diversity and limnological characterization in two shallow tropical urban reservoirs of Pernambuco State, Brazil
Methods of data collection in qualitative research: Interviews and focus groups
This paper explores the most common methods of data collection used in qualitative research: interviews and focus groups. The paper examines each method in detail, focusing on how they work in practice, when their use is appropriate and what they can offer dentistry. Examples of empirical studies that have used interviews or focus groups are also provided