2,677 research outputs found

    Driving Towards Success in the Air Force Cyber Mission: Leveraging Our Heritage to Shape Our Future

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    Ongoing debates address what constitutes cyber warfare and whether or not we really are at war in cyberspace. This article does not enter into those issues; rather, it suggests how the Air Force and Air University should move forward to lead and support our nation’s cyber security needs. Thus, it focuses on analogous lessons learned from history, our position today and what it needs to be, and plans for getting there with respect to our cyberspace capabilities

    Phagocyte receptors for apoptotic cells: recognition, uptake, and consequences

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    Mass spectrometry strategies to unveil modified aminophospholipids of biological interest

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    The biological functions of modified aminophospholipids (APL) have become a topic of interest during the last two decades, and distinct roles have been found for these biomolecules in both physiological and pathological contexts. Modifications of APL include oxidation, glycation, and adduction to electrophilic aldehydes, altogether contributing to a high structural variability of modified APL. An outstanding technique used in this challenging field is mass spectrometry (MS). MS has been widely used to unveil modified APL of biological interest, mainly when associated with soft ionization methods (electrospray and matrix-assisted laser desorption ionization) and coupled with separation techniques as liquid chromatography. This review summarizes the biological roles and the chemical mechanisms underlying APL modifications, and comprehensively reviews the current MS-based knowledge that has been gathered until now for their analysis. The interpretation of the MS data obtained by in vitro-identification studies is explained in detail. The perspective of an analytical detection of modified APL in clinical samples is explored, highlighting the fundamental role of MS in unveiling APL modifications and their relevance in pathophysiology.publishe

    A Hierarchical Role for Classical Pathway Complement Proteins in the Clearance of Apoptotic Cells in Vivo

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    The strongest susceptibility genes for the development of systemic lupus erythematosus (SLE) in humans are null mutants of classical pathway complement proteins. There is a hierarchy of disease susceptibility and severity according to the position of the missing protein in the activation pathway, with the severest disease associated with C1q deficiency. Here we demonstrate, using novel in vivo models of apoptotic cell clearance during sterile peritonitis, a similar hierarchical role for classical pathway complement proteins in vivo in the clearance of apoptotic cells by macrophages. Our results constitute the first demonstration of an impairment in the phagocytosis of apoptotic cells by macrophages in vivo in a mammalian system. Apoptotic cells are thought to be a major source of the autoantigens of SLE, and impairment of their removal by complement may explain the link between hereditary complement deficiency and the development of SLE

    Current understanding of the mechanisms for clearance of apoptotic cells-a fine balance

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    Apoptosis is an important cell death mechanism by which multicellular organisms remove unwanted cells. It culminates in a rapid, controlled removal of cell corpses by neighboring or recruited viable cells. Whilst many of the molecular mechanisms that mediate corpse clearance are components of the innate immune system, clearance of apoptotic cells is an anti-inflammatory process. Control of cell death is dependent on competing pro-apoptotic and anti-apoptotic signals. Evidence now suggests a similar balance of competing signals is central to the effective removal of cells, through so called 'eat me' and 'don't eat me' signals. Competing signals are also important for the controlled recruitment of phagocytes to sites of cell death. Consequently recruitment of phagocytes to and from sites of cell death can underlie the resolution or inappropriate propagation of cell death and inflammation. This article highlights our understanding of mechanisms mediating clearance of dying cells and discusses those mechanisms controlling phagocyte migration and how inappropriate control may promote important pathologies. © the authors, publisher and licensee libertas academica limited
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