481 research outputs found

    Heat Transfer Characteristics of Regenerator Matrix (Case of Packed Wire Gauzes)

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    The average heat transfer coefficient in the matrix of laminated wire screens (10 to 250 mesh) for a Stirling engine heat exchanger was studied experimentally. The data are correlated by N sub ud = 0.42 R sub ed 0.56 (3 or = R sub ed or = 400), and R sub ed are the Nusselt and Reynolds nubmers based on the wire diameter. The pressure drop decreased and the heat transfer increased as the wire diameter was decreased

    Concepts of GPCR-controlled navigation in the immune system

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    G-protein-coupled receptor (GPCR) signaling is essential for the spatiotemporal control of leukocyte dynamics during immune responses. For efficient navigation through mammalian tissues, most leukocyte types express more than one GPCR on their surface and sense a wide range of chemokines and chemoattractants, leading to basic forms of leukocyte movement (chemokinesis, haptokinesis, chemotaxis, haptotaxis, and chemorepulsion). How leukocytes integrate multiple GPCR signals and make directional decisions in lymphoid and inflamed tissues is still subject of intense research. Many of our concepts on GPCR-controlled leukocyte navigation in the presence of multiple GPCR signals derive from in vitro chemotaxis studies and lower vertebrates. In this review, we refer to these concepts and critically contemplate their relevance for the directional movement of several leukocyte subsets (neutrophils, T cells, and dendritic cells) in the complexity of mouse tissues. We discuss how leukocyte navigation can be regulated at the level of only a single GPCR (surface expression, competitive antagonism, oligomerization, homologous desensitization, and receptor internalization) or multiple GPCRs (synergy, hierarchical and non-hierarchical competition, sequential signaling, heterologous desensitization, and agonist scavenging). In particular, we will highlight recent advances in understanding GPCR-controlled leukocyte navigation by intravital microscopy of immune cells in mice

    Photoproduction of Lambda(1405) and Sigma^{0}(1385) on the proton at E_\gamma = 1.5-2.4 GeV

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    Differential cross sections for γpK+Λ(1405)\gamma p \to K^+\Lambda(1405) and γpK+Σ0(1385)\gamma p \to K^+\Sigma^0(1385) reactions have been measured in the photon energy range from 1.5 to 2.4 GeV and the angular range of 0.8<cos(Θ)<1.00.8<\cos(\Theta)<1.0 for the K+K^+ scattering angle in the center-of-mass system. This data is the first measurement of the Λ(1405)\Lambda(1405) photoproduction cross section. The lineshapes of \LamS measured in Σ+π\Sigma^+\pi^- and Σπ+\Sigma^-\pi^+ decay modes were different with each other, indicating a strong interference of the isospin 0 and 1 terms of the Σπ\Sigma\pi scattering amplitudes. The ratios of \LamS production to \SigS production were measured in two photon energy ranges: near the production threshold (1.5<Eγ<2.01.5<E_\gamma<2.0 GeV) and far from it (2.0<Eγ<2.42.0 <E_\gamma<2.4 GeV). The observed ratio decreased in the higher photon energy region, which may suggest different production mechanisms and internal structures for these hyperon resonances

    Optical pumping NMR in the compensated semiconductor InP:Fe

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    The optical pumping NMR effect in the compensated semiconductor InP:Fe has been investigated in terms of the dependences of photon energy (E_p), helicity (sigma+-), and exposure time (tau_L) of infrared lights. The {31}P and {115}In signal enhancements show large sigma+- asymmetries and anomalous oscillations as a function of E_p. We find that (i) the oscillation period as a function of E_p is similar for {31}P and {115}In and almost field independent in spite of significant reduction of the enhancement in higher fields. (ii) A characteristic time for buildup of the {31}P polarization under the light exposure shows strong E_p-dependence, but is almost independent of sigma+-. (iii) The buildup times for {31}P and {115}In are of the same order (10^3 s), although the spin-lattice relaxation times (T_1) are different by more than three orders of magnitude between them. The results are discussed in terms of (1) discrete energy spectra due to donor-acceptor pairs (DAPs) in compensated semiconductors, and (2) interplay between {31}P and dipolar ordered indium nuclei, which are optically induced.Comment: 8 pages, 6 figures, submitted to Physical Review

    Two-particle interference of electron pairs on a molecular level

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    We investigate the photo-doubleionization of H2H_2 molecules with 400 eV photons. We find that the emitted electrons do not show any sign of two-center interference fringes in their angular emission distributions if considered separately. In contrast, the quasi-particle consisting of both electrons (i.e. the "dielectron") does. The work highlights the fact that non-local effects are embedded everywhere in nature where many-particle processes are involved

    Checkpoints are blind to replication restart and recombination intermediates that result in gross chromosomal rearrangements

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    Replication fork inactivation can be overcome by homologous recombination, but this can cause gross chromosomal rearrangements that subsequently missegregate at mitosis, driving further chromosome instability. It is unclear when the chromosome rearrangements are generated and whether individual replication problems or the resulting recombination intermediates delay the cell cycle. Here we have investigated checkpoint activation during HR-dependent replication restart using a site-specific replication fork-arrest system. Analysis during a single cell cycle shows that HR-dependent replication intermediates arise in S phase, shortly after replication arrest, and are resolved into acentric and dicentric chromosomes in G2. Despite this, cells progress into mitosis without delay. Neither the DNA damage nor the intra-S phase checkpoints are activated in the first cell cycle, demonstrating that these checkpoints are blind to replication and recombination intermediates as well as to rearranged chromosomes. The dicentrics form anaphase bridges that subsequently break, inducing checkpoint activation in the second cell cycle
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