1,329 research outputs found

    A rhetorical analysis of the address of Governor George C Wallace delivered during the third-party state convention held in Omaha, Nebraska, on March 4, 1968

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    When George Corley Wallace, twice governor of Alabama and militant advocate for states’ rights and segregation, collected enough signatures to put his American Independent Party on the 1968 ballot for the Presidential race, there emerged on the political scene what many people called a phenomenon, and extraordinary happening or circumstance. It appeared that for a time many observers had considered him only a faintly comical entry. But now George Wallace became a rival who threatened to jostle all political candidates. Nationwide polls certified him as a possible spoiler, and more was his “pull” that tripled his appeal outside the South. Both major parties now had to concern themselves with the new political arithmetic created by Wallace who expected to be on the ballot in nearly all fifty states. It was estimated that Wallace would probably take more votes away from Republicans than from Democrats, and in this new situation every White House aspirant was busy adding up his own special qualifications to blunt the Wallace raid. Wallace conducted a remarkable and sometimes destructive campaign which began in his own state of Alabama, continued throughout many of the southern states, and then progressed to the other sections of the United States. When the final ballot for President of the United States was over, Wallace carried five states in the Deep South: Alabama, Arkansas, Georgia, Louisiana, and Mississippi. Although he conducted a national campaign, he did not carry any of the border states or southwestern states, or any states in the North. The Wallace phenomenon was felt by the Democratic and Republican Parties, and for a time, columnist, politicians, and other political observers expressed fears of a third party deadlock of the election

    The Development of an Employee Wellness Program Within a Mid-Sized Company

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    INTRODUCTION: With over 160 million Americans currently in the workforce, employee wellness programs have proven to be a viable method of reaching a large population with an objective of improving health outcomes. These programs can encourage the awareness of health-related issues including nutrition, physical activity, preventative health screening, and stress management, and they also can serve to improve employee morale and/or engagement. Moreover, they can often help to reduce healthcare costs to both the organization and the individual employees. AIM: The purpose of this capstone was to design a framework for an employee wellness program that could be utilized within a mid-sized private logistics company with multiple locations across the United States. METHODS: The program was developed using the Precede portion of the PRECEDE-PROCEED model as the guiding framework. An essential first step of the program development involved a synthesis of published evidence involving published reports, reviews, and evaluations of other previously implemented worksite wellness initiatives. RESULTS: A worksite wellness plan was proposed for a midsize company that addresses incentive policies, environmental changes, and recommended health education and behavioral structures for enhanced health and wellness among a workforce of approximately 800 employees. DISCUSSION: The Proceed model steps will ensure a comprehensive evaluation of the program’s immediate impacts and long-term outcomes over time. It is important that the short, medium, and long term goals of the program are identified so that an evaluation process can be implemented to see if these specific objectives are met through the initiatives implemented in the program

    Trauma and repetition : an intersubjective perspective

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    Includes bibliographical references (leaves 98-108).This research study employed the single case-study method with the aim of illustrating how extraordinarily difficult it can be within a South African context to name racial, gender and class differences and their concomitant painful histories within the therapeutic space. The evolution of trauma is followed with particular emphasis on its relationship to gender. This case study focuses particularly on the intersubjective space generated between a White, male intern psychologist and a Coloured, female survivor of gender based violence. Material gathered over an eleven-month treatment period highlighted a resistance of both parties to acknowledge and engage with issues, such as race and gender, which threatened both client and therapist with early traumatogenetic repetitions within the therapeutic space

    Transcriptional Suppression of Interleukin-12 Gene Expression following Phagocytosis of Apoptotic Cells

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    AbstractPhagocytosis of apoptotic cells usually results in an anti-inflammatory state with inhibition of proinflammatory cytokines such as IL-12. How apoptotic cell-derived signals regulate IL-12 gene expression is not understood. We demonstrate that cell-cell contact with apoptotic cells is sufficient to induce profound inhibition of IL-12 production by activated macrophages. Phosphatidylserine could mimic the inhibitory effect. The inhibition does not involve autocrine or paracrine actions of IL-10 and TGF-β. We report the identification, purification, and cloning of a novel zinc finger nuclear factor, named GC binding protein (GC-BP), that is induced following phagocytosis of apoptotic cells by macrophages or by treatment with phosphatidylserine. GC-BP selectively inhibits IL-12 p35 gene transcription by binding to its promoter in vitro and in vivo, thus decreasing IL-12 production. Blocking GC-BP by RNA interference restores IL-12 p35 transcription and IL-12 p70 synthesis. Finally, GC-BP itself undergoes functionally significant tyrosine dephosphorylation in response to apoptotic cells

    Autoantibodies make a U-turn: the toll hypothesis for autoantibody specificity

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    Like the immune response itself, our efforts to understand the “rules” for self–nonself discrimination are constantly evolving. The discovery of pattern recognition receptors—the Toll-like receptor (TLR) family in particular—shifted the emphasis of self–nonself recognition from lymphocytes functioning in the adaptive immune system to antigen-presenting cells (APCs) functioning in the innate immune system. Two new articles, one in a recent issue (1) and one in this issue (see Vollmer et al. [2] on p. 1575), demonstrate that antigen–antibody complexes containing RNAs activate B lymphocytes and dendritic cells (DCs) through interaction with TLR7 and/or TLR8. From these and other papers, one begins to see how specific types of autoantigens—by virtue of their capacity to act as TLR ligands—favor autoantibody production. This is known as the Toll hypothesis

    Major role for mRNA stability in shaping the kinetics of gene induction

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    <p>Abstract</p> <p>Background</p> <p>mRNA levels in cells are determined by the relative rates of RNA production and degradation. Yet, to date, most analyses of gene expression profiles were focused on mechanisms which regulate transcription, while the role of mRNA stability in modulating transcriptional networks was to a large extent overlooked. In particular, kinetic waves in transcriptional responses are usually interpreted as resulting from sequential activation of transcription factors.</p> <p>Results</p> <p>In this study, we examined on a global scale the role of mRNA stability in shaping the kinetics of gene response. Analyzing numerous expression datasets we revealed a striking global anti-correlation between rapidity of induction and mRNA stability, fitting the prediction of a kinetic mathematical model. In contrast, the relationship between kinetics and stability was less significant when gene suppression was analyzed. Frequently, mRNAs that are stable under standard conditions were very rapidly down-regulated following stimulation. Such effect cannot be explained even by a complete shut-off of transcription, and therefore indicates intense modulation of RNA stability.</p> <p>Conclusion</p> <p>Taken together, our results demonstrate the key role of mRNA stability in determining induction kinetics in mammalian transcriptional networks.</p

    Functional genomic delineation of TLR-induced transcriptional networks

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    <p>Abstract</p> <p>Background</p> <p>The innate immune system is the first line of defense mechanisms protecting the host from invading pathogens such as bacteria and viruses. The innate immunity responses are triggered by recognition of prototypical pathogen components by cellular receptors. Prominent among these pathogen sensors are Toll-like receptors (TLRs). We sought global delineation of transcriptional networks induced by TLRs, analyzing four genome-wide expression datasets in mouse and human macrophages stimulated with pathogen-mimetic agents that engage various TLRs.</p> <p>Results</p> <p>Combining computational analysis of expression profiles and cis-regulatory promoter sequences, we dissected the TLR-induced transcriptional program into two major components: the first is universally activated by all examined TLRs, and the second is specific to activated TLR3 and TLR4. Our results point to NF-ÎşB and ISRE-binding transcription factors as the key regulators of the universal and the TLR3/4-specific responses, respectively, and identify novel putative positive and negative feedback loops in these transcriptional programs. Analysis of the kinetics of the induced network showed that while NF-ÎşB regulates mainly an early-induced and sustained response, the ISRE element functions primarily in the induction of a delayed wave. We further demonstrate that co-occurrence of the NF-ÎşB and ISRE elements in the same promoter endows its targets with enhanced responsiveness.</p> <p>Conclusion</p> <p>Our results enhance system-level understanding of the networks induced by TLRs and demonstrate the power of genomics approaches to delineate intricate transcriptional webs in mammalian systems. Such systems-level knowledge of the TLR network can be useful for designing ways to pharmacologically manipulate the activity of the innate immunity in pathological conditions in which either enhancement or repression of this branch of the immune system is desired.</p
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