942 research outputs found

    Sharp Estimates of the Embedding Constants for Besov Spaces

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    Sharp estimates are obtained for the rates of blow up of the norms of embeddings of Besov spaces in Lorentz spaces as the parameters approach critical values.Sharp estimates are obtained for the rates of blow up of the norms of embeddings of Besov spaces in Lorentz spaces as the parameters approach critical values

    Sharp Estimates of the Embedding Constants for Besov Spaces bs p,q, 0 < p < 1

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    Sharp estimates are obtained for the rates of blow up of the norms of embeddings of Besov spaces bs p,q in Lorentz spaces as the parameters approach critical values. In [8] the case 1 _ p < 1 was investigated. The case 0 < p < 1 of the present paper requires different methods as the pointwise estimates established are different and the interpolation argument used in [8] is no longer available

    Evaluation of an ambulatory system for the quantification of cough frequency in patients with chronic obstructive pulmonary disease

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    BACKGROUND: To date, methods used to assess cough have been primarily subjective, and only broadly reflect the impact of chronic cough and/or chronic cough therapies on quality of life. Objective assessment of cough has been attempted, but early techniques were neither ambulatory nor feasible for long-term data collection. We evaluated a novel ambulatory cardio-respiratory monitoring system with an integrated unidirectional, contact microphone, and report here the results from a study of patients with COPD who were videotaped in a quasi-controlled environment for 24 continuous hours while wearing the ambulatory system. METHODS: Eight patients with a documented history of COPD with ten or more years of smoking (6 women; age 57.4 ± 11.8 yrs.; percent predicted FEV(1 )49.6 ± 13.7%) who complained of cough were evaluated in a clinical research unit equipped with video and sound recording capabilities. All patients wore the LifeShirt(® )system (LS) while undergoing simultaneous video (with sound) surveillance. Video data were visually inspected and annotated to indicate all cough events. Raw physiologic data records were visually inspected by technicians who remained blinded to the video data. Cough events from LS were analyzed quantitatively with a specialized software algorithm to identify cough. The output of the software algorithm was compared to video records on a per event basis in order to determine the validity of the LS system to detect cough in COPD patients. RESULTS: Video surveillance identified a total of 3,645 coughs, while LS identified 3,363 coughs during the same period. The median cough rate per patient was 21.3 coughs·hr(-1 )(Range: 10.1 cghs·hr(-1 )– 59.9 cghs·hr(-1)). The overall accuracy of the LS system was 99.0%. Overall sensitivity and specificity of LS, when compared to video surveillance, were 0.781 and 0.996, respectively, while positive- and negative-predictive values were 0.846 and 0.994. There was very good agreement between the LS system and video (kappa = 0.807). CONCLUSION: The LS system demonstrated a high level of accuracy and agreement when compared to video surveillance for the measurement of cough in patients with COPD

    A CD4+ T cell antagonist epitope down-regulates activating signaling proteins, up-regulates inhibitory signaling proteins and abrogates HIV-specific T cell function

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    BACKGROUND: CD4(+) T cells are critically important in HIV infection, being both the primary cells infected by HIV and likely playing a direct or indirect role in helping control virus replication. Key areas of interest in HIV vaccine research are mechanisms of viral escape from the immune response. Interestingly, in HIV infection it has been shown that peptide sequence variation can reduce CD4(+) T cell responses to the virus, and small changes to peptide sequences can transform agonist peptides into antagonist peptides. RESULTS: We describe, at a molecular level, the consequences of antagonism of HIV p24-specific CD4(+) T cells. Antagonist peptide exposure in the presence of agonist peptide caused a global suppression of agonist-induced gene expression and signaling molecule phosphorylation. In addition to down-regulation of factors associated with T cell activation, a smaller subset of genes associated with negative regulation of cell activation was up-regulated, including KFL-2, SOCS-1, and SPDEY9P. Finally, antagonist peptide in the absence of agonist peptide also delivered a negative signal to T cells. CONCLUSIONS: Small changes in p24-specific peptides can result in T cell antagonism and reductions of both T cell receptor signaling and activation. These changes are at least in part mediated by a dominant negative signal delivered by antagonist peptide, as evidenced by up-regulation of negative regulatory genes in the presence of agonist plus antagonist stimulation. Antagonism can have dramatic effects on CD4(+) T cell function and presents a potential obstacle to HIV vaccine development
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