694 research outputs found

    Parity Violation in Proton-Proton Scattering at 221 MeV

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    The parity-violating longitudinal analyzing power, Az, has been measured in pp elastic scattering at an incident proton energy of 221 MeV. The result obtained is Az =(0.84 +/- 0.29 (stat.) +/- 0.17 (syst.)) x 10^{-7}. This experiment is unique in that it selects a single parity violating transition amplitude, 3P2-1D2, and consequently directly constrains the weak meson-nucleon coupling constant h^pp_rho When this result is taken together with the existing pp parity violation data, the weak meson-nucleon coupling constants h^pp_rho and h^pp_omega can, for the first time, both be determined.Comment: 8 pages RevTeX4, 3 PostScript figures. Conclusion revised. New information about weak coupling constants adde

    Parity Violation in Proton-Proton Scattering at 221 MeV

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    TRIUMF experiment 497 has measured the parity violating longitudinal analyzing power, A_z, in pp elastic scattering at 221.3 MeV incident proton energy. This paper includes details of the corrections, some of magnitude comparable to A_z itself, required to arrive at the final result. The largest correction was for the effects of first moments of transverse polarization. The addition of the result, A_z=(0.84 \pm 0.29 (stat.) \pm 0.17 (syst.)) \times 10^{-7}, to the pp parity violation experimental data base greatly improves the experimental constraints on the weak meson-nucleon coupling constants h^{pp}_\rho and h^{pp}_\omega, and has implications for the interpretation of electron parity violation experiments.Comment: 17 pages RevTeX, 14 PostScript figures. Revised version with additions suggested by Phys. Rev.

    The major histocompatibility complex homozygous inbred Babraham pig as a resource for veterinary and translational medicine

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    The Babraham pig is a highly inbred breed first developed in the United Kingdom approximately 50 years ago. Previous reports indicate a very high degree of homozygosity across the genome, including the major histocompatibility complex (MHC) region, but confirmation of homozygosity at the specific MHC loci was lacking. Using both direct sequencing and PCR‐based sequence‐specific typing, we confirm that Babraham pigs are essentially homozygous at their MHC loci and formalise their MHC haplotype as Hp‐55.6. This enhances the utility of the Babraham pig as a useful biomedical model for studies in which controlling for genetic variation is important

    Marx’s "Capital"in the Information Age

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    This article argues that a media and communication studies perspective on reading Marx’s Capital has thus far been missing, but is needed in the age of information capitalism and digital capitalism. Two of the most popular contemporary companions to Marx’s Capital, the ones by David Harvey and Michael Heinrich, present themselves as general guidebooks on how to read Marx, but are actually biased towards particular schools of Marxist thought. A contemporary reading of Marx needs to be mediated with contemporary capitalism’s structures and the political issues of the day. Media, communications and the Internet are important issues for such a reading today. It is time to see Marx not just as a critic of capitalism but also as a critic of capitalist communications

    Accumulating discursive capital, valuating subject positions. From Marx to Foucault

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    Whenever people use language, they participate in valuation practices, i.e. they give value to themselves as well as to others. To account for the construction of social inequality through discursive valuation practices, discourse theorists need Marxist theory and Marxists need discourse theory. By going from the early Marx to the late Foucault, I will revisit Marx?s value theory in light of practice-oriented approaches to social inequality. I will discuss examples from two distinct arenas, the monopolization of attention by populist leaders and the academic star system, both of which are accounted for in terms of the accumulation of discursive capital. This perspective asks how the value of subject positions is constructed and hierarchies between them are established in discursive practices. Investigating the construction of valuable subject positions in discourse communities, this perspective attempts to overcome the traditional division between language, the economic and the social. Discourse not only represents value and the social order but, through representation, it also contributes to constituting the social as a hierarchical world of more or less valued subject positions

    Contribution of DEAF1 Structural Domains to the Interaction with the Breast Cancer Oncogene LMO4

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    The proteins LMO4 and DEAF1 contribute to the proliferation of mammary epithelial cells. During breast cancer LMO4 is upregulated, affecting its interaction with other protein partners. This may set cells on a path to tumour formation. LMO4 and DEAF1 interact, but it is unknown how they cooperate to regulate cell proliferation. In this study, we identify a specific LMO4-binding domain in DEAF1. This domain contains an unstructured region that directly contacts LMO4, and a coiled coil that contains the DEAF1 nuclear export signal (NES). The coiled coil region can form tetramers and has the typical properties of a coiled coil domain. Using a simple cell-based assay, we show that LMO4 modulates the activity of the DEAF NES, causing nuclear accumulation of a construct containing the LMO4-interaction region of DEAF1

    Oncogenic LMO3 Collaborates with HEN2 to Enhance Neuroblastoma Cell Growth through Transactivation of Mash1

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    Expression of Mash1 is dysregulated in human neuroblastoma. We have also reported that LMO3 (LIM-only protein 3) has an oncogenic potential in collaboration with neuronal transcription factor HEN2 in neuroblastoma. However, the precise molecular mechanisms of its transcriptional regulation remain elusive. Here we found that LMO3 forms a complex with HEN2 and acts as an upstream mediator for transcription of Mash1 in neuroblastoma. The high levels of LMO3 or Mash1 mRNA expression were significantly associated with poor prognosis in 100 primary neuroblastomas. The up-regulation of Mash1 remarkably accelerated the proliferation of SH-SY5Y neuroblastoma cells, while siRNA-mediated knockdown of LMO3 induced inhibition of growth of SH-SY5Y cells in association with a significant down-regulation of Mash1. Additionally, overexpression of both LMO3 and HEN2 induced expression of Mash1, suggesting that they might function as a transcriptional activator for Mash1. Luciferase reporter assay demonstrated that the co-expression of LMO3 and HEN2 attenuates HES1 (a negative regulator for Mash1)-dependent reduction of luciferase activity driven by the Mash1 promoter. Chromatin immunoprecipitation assay revealed that LMO3 and HEN2 reduce the amount of HES1 recruited onto putative HES1-binding sites and E-box within the Mash1 promoter. Furthermore, both LMO3 and HEN2 are physically associated with HES1 by immunoprecipitation assay. Thus, our present results suggest that a transcriptional complex of LMO3 and HEN2 may contribute to the genesis and malignant phenotype of neuroblastoma by inhibiting HES1 which suppresses the transactivation of Mash1

    Automatic segmentation of myocardium from black-blood MR images using entropy and local neighborhood information.

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    By using entropy and local neighborhood information, we present in this study a robust adaptive Gaussian regularizing Chan-Vese (CV) model to segment the myocardium from magnetic resonance images with intensity inhomogeneity. By utilizing the circular Hough transformation (CHT) our model is able to detect epicardial and endocardial contours of the left ventricle (LV) as circles automatically, and the circles are used as the initialization. In the cost functional of our model, the interior and exterior energies are weighted by the entropy to improve the robustness of the evolving curve. Local neighborhood information is used to evolve the level set function to reduce the impact of the heterogeneity inside the regions and to improve the segmentation accuracy. An adaptive window is utilized to reduce the sensitivity to initialization. The Gaussian kernel is used to regularize the level set function, which can not only ensure the smoothness and stability of the level set function, but also eliminate the traditional Euclidean length term and re-initialization. Extensive validation of the proposed method on patient data demonstrates its superior performance over other state-of-the-art methods

    Expression of cytokine and chemokine mRNA and secretion of tumor necrosis factor-Ξ± by gallbladder epithelial cells: Response to bacterial lipopolysaccharides

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    BACKGROUND: In addition to immune cells, many other cell types are known to produce cytokines. Cultured normal mouse gallbladder epithelial cells, used as a model system for gallbladder epithelium, were examined for their ability to express the mRNA of various cytokines and chemokines in response to bacterial lipopolysaccharide. The synthesis and secretion of the tumor necrosis factor-Ξ± (TNF-Ξ±) protein by these cells was also measured. RESULTS: Untreated mouse gallbladder cells expressed mRNA for TNF-Ξ±, RANTES, and macrophage inflammatory protein-2 (MIP-2). Upon treatment with lipopolysaccharide, these cells now produced mRNA for Interleukin-1Ξ² (IL-1Ξ²), IL-6, monocyte chemoattractant protein-1 (MCP-1), and showed increased expression of TNF-Ξ± and MIP-2 mRNA. Untreated mouse gallbladder cells did not synthesize TNF-Ξ± protein; however, they did synthesize and secrete TNF-Ξ± upon treatment with lipopolysaccharide. METHODS: Cells were treated with lipopolysaccharides from 3 strains of bacteria. Qualitative and semi-quantitative RT-PCR, using cytokine or chemokine-specific primers, was used to measure mRNA levels of TNFΞ±, IL-1Ξ², IL-6, IL-10, KC, RANTES, MCP-1, and MIP-2. TNF-Ξ± protein was measured by immunoassays. CONCLUSION: This research demonstrates that gallbladder epithelial cells in response to lipopolysaccharide exposure can alter their cytokine and chemokine RNA expression pattern and can synthesize and secrete TNFΞ± protein. This suggests a mechanism whereby gallbladder epithelial cells in vivo may mediate gallbladder secretory function, inflammation and diseases in an autocrine/paracrine fashion by producing and secreting cytokines and/or chemokines during sepsis
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