948 research outputs found

    Continuous-wave cavity ringdown spectroscopy of the 8 nu polyad of water in the 25 195-25 340 cm(-1) range

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    State-of-the-art experiments and calculations are used to record and assign the data obtained in the weakly absorbing blue energy region of the H2O spectrum. Continuous-wave cavity ringdown absorption spectroscopy with Doppler resolution is used to probe the range from 25 195 to 25 470 cm(-1) with an absorption sensitivity of similar to 1 parts per 10(9) (ppb)/cm. 62 lines of the polyad nu(OH)=8 are reported, of which 43 are assigned using variational nuclear calculations. The study includes absorption line intensities (in the range of 10(-28)-10(-26) cm/molecule) for all lines and self-broadening pressure coefficient for a few lines. The newly obtained energy levels are also reported. (c) 2005 American Institute of Physics

    Decision and Discovery in Defining “Disease”

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    This version (May 17, 2005) was published in its final form as: Schwartz PH. Decision and discovery in defining 'disease'. In: Kincaid H, McKitrick J, editors. Establishing medical reality: essays in the metaphysics and epistemology of biomedical science. Dordrecht: Springer; 2007. p. 47-63. http://dx.doi.org/10.1007/1-4020-5216-2_5The debate over how to analyze the concept of disease has often centered on the question of whether to include a reference to values, in particular the ‘disvalue’of diseases, or whether to avoid such notions. ‘Normativists,’such as King ([1954], 1981) and Culver and Gert (1982) emphasize the undesirability of diseases, while ‘Naturalists,’ most prominently Christopher Boorse (1977, 1987, 1997), instead require just the presence of biological dysfunction. The debate between normativism and naturalism often deteriorates into stalemate, with each side able to point out significant problems with the other. It starts to look as if neither approach can work. In this paper, I argue that the standoff stems from deeply questionable assumptions that have been used to formulate the opposing positions and guide the debate. In the end, I propose an alternative set of guidelines that offer a more constructive way to devise and compare theories

    Medium Modifications of Hadron Properties and Partonic Processes

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    Chiral symmetry is one of the most fundamental symmetries in QCD. It is closely connected to hadron properties in the nuclear medium via the reduction of the quark condensate , manifesting the partial restoration of chiral symmetry. To better understand this important issue, a number of Jefferson Lab experiments over the past decade have focused on understanding properties of mesons and nucleons in the nuclear medium, often benefiting from the high polarization and luminosity of the CEBAF accelerator. In particular, a novel, accurate, polarization transfer measurement technique revealed for the first time a strong indication that the bound proton electromagnetic form factors in 4He may be modified compared to those in the vacuum. Second, the photoproduction of vector mesons on various nuclei has been measured via their decay to e+e- to study possible in-medium effects on the properties of the rho meson. In this experiment, no significant mass shift and some broadening consistent with expected collisional broadening for the rho meson has been observed, providing tight constraints on model calculations. Finally, processes involving in-medium parton propagation have been studied. The medium modifications of the quark fragmentation functions have been extracted with much higher statistical accuracy than previously possible.Comment: to appear in J. Phys.: Conf. Proc. "New Insights into the Structure of Matter: The First Decade of Science at Jefferson Lab", eds. D. Higinbotham, W. Melnitchouk, A. Thomas; added reference

    Alterations in the transcriptome and antibiotic susceptibility of Staphylococcus aureus grown in the presence of diclofenac

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    <p>Abstract</p> <p>Background</p> <p>Diclofenac is a non-steroidal anti-inflammatory drug (NSAID) which has been shown to increase the susceptibility of various bacteria to antimicrobials and demonstrated to have broad antimicrobial activity. This study describes transcriptome alterations in <it>S. aureus </it>strain COL grown with diclofenac and characterizes the effects of this NSAID on antibiotic susceptibility in laboratory, clinical and diclofenac reduced-susceptibility (Dc<sup>RS</sup>) <it>S. aureus </it>strains.</p> <p>Methods</p> <p>Transcriptional alterations in response to growth with diclofenac were measured using <it>S. aureus </it>gene expression microarrays and quantitative real-time PCR. Antimicrobial susceptibility was determined by agar diffusion MICs and gradient plate analysis. Ciprofloxacin accumulation was measured by fluorescence spectrophotometry.</p> <p>Results</p> <p>Growth of <it>S. aureus </it>strain COL with 80 μg/ml (0.2 × MIC) of diclofenac resulted in the significant alteration by ≥2-fold of 458 genes. These represented genes encoding proteins for transport and binding, protein and DNA synthesis, and the cell envelope. Notable alterations included the strong down-regulation of antimicrobial efflux pumps including <it>mepRAB </it>and a putative <it>emrAB/qacA</it>-family pump. Diclofenac up-regulated <it>sigB </it>(σ<sup>B</sup>), encoding an alternative sigma factor which has been shown to be important for antimicrobial resistance. <it>Staphylococcus aureus </it>microarray metadatabase (SAMMD) analysis further revealed that 46% of genes differentially-expressed with diclofenac are also σ<sup>B</sup>-regulated. Diclofenac altered <it>S. aureus </it>susceptibility to multiple antibiotics in a strain-dependent manner. Susceptibility increased for ciprofloxacin, ofloxacin and norfloxacin, decreased for oxacillin and vancomycin, and did not change for tetracycline or chloramphenicol. Mutation to Dc<sup>RS </sup>did not affect susceptibility to the above antibiotics. Reduced ciprofloxacin MICs with diclofenac in strain BB255, were not associated with increased drug accumulation.</p> <p>Conclusions</p> <p>The results of this study suggest that diclofenac influences antibiotic susceptibility in <it>S. aureus</it>, in part, by altering the expression of regulatory and structural genes associated with cell wall biosynthesis/turnover and transport.</p

    Alterations In the Transciptome and Antibiotic Susceptibility of \u3ci\u3eStaphylococcus aureus\u3c/i\u3e Grown In the Presence of Diclofenac

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    Background Diclofenac is a non-steroidal anti-inflammatory drug (NSAID) which has been shown to increase the susceptibility of various bacteria to antimicrobials and demonstrated to have broad antimicrobial activity. This study describes transcriptome alterations in S. aureus strain COL grown with diclofenac and characterizes the effects of this NSAID on antibiotic susceptibility in laboratory, clinical and diclofenac reduced-susceptibility (DcRS) S. aureus strains. Methods Transcriptional alterations in response to growth with diclofenac were measured using S. aureus gene expression microarrays and quantitative real-time PCR. Antimicrobial susceptibility was determined by agar diffusion MICs and gradient plate analysis. Ciprofloxacin accumulation was measured by fluorescence spectrophotometry. Results Growth of S. aureus strain COL with 80 μg/ml (0.2 × MIC) of diclofenac resulted in the significant alteration by ≥2-fold of 458 genes. These represented genes encoding proteins for transport and binding, protein and DNA synthesis, and the cell envelope. Notable alterations included the strong down-regulation of antimicrobial efflux pumps including mepRAB and a putative emrAB/qacA-family pump. Diclofenac up-regulated sigB (σB), encoding an alternative sigma factor which has been shown to be important for antimicrobial resistance. Staphylococcus aureus microarray metadatabase (SAMMD) analysis further revealed that 46% of genes differentially-expressed with diclofenac are also σB-regulated. Diclofenac altered S. aureus susceptibility to multiple antibiotics in a strain-dependent manner. Susceptibility increased for ciprofloxacin, ofloxacin and norfloxacin, decreased for oxacillin and vancomycin, and did not change for tetracycline or chloramphenicol. Mutation to DcRS did not affect susceptibility to the above antibiotics. Reduced ciprofloxacin MICs with diclofenac in strain BB255, were not associated with increased drug accumulation. Conclusions The results of this study suggest that diclofenac influences antibiotic susceptibility in S. aureus, in part, by altering the expression of regulatory and structural genes associated with cell wall biosynthesis/turnover and transport
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