57 research outputs found

    Analysis of Kaon Production at SIS Energies

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    We analyse the production and propagation of pions and kaons in heavy-ion reactions from 0.8 -- 1.8~A⋅\cdotGeV within a coupled channel transport approach including the kaon production channels BB→K+YN,πB→K+Y,BB→NNKKˉ,πB→NKKˉ,K+B→K+BBB \to K^+YN, \pi B\to K^+Y, BB \to NN K \bar{K}, \pi B\to N K\bar{K}, K^+B\to K^+B and ππ→KKˉ\pi \pi\to K \bar{K}. Assuming the hyperon selfenergy to be 2/3 of the nucleon selfenergy we find that all inclusive experimental K+K^+ spectra at SIS energies can be reproduced reasonably well without any selfenergies for the kaons although a slightly repulsive kaon potential cannot be excluded by the present data on kaon spectra and flow.Comment: 19 pages, LaTeX, including 8 postscript figures, to appear in Nucl. Phys.

    Antiflow of kaons in relativistic heavy ion collisions

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    We compare relativistic transport model calculations to recent data on the sideward flow of neutral strange K^0_s mesons for Au+Au collisions at 6 AGeV. A soft nuclear equation of state is found to describe very well the positive proton flow data measured in the same experiment. In the absence of kaon potential, the K^0 flow pattern is similar to that of protons. The kaon flow becomes negative if a repulsive kaon potential determined from the impulse approximation is introduced. However, this potential underestimates the data which exhibits larger antiflow. An excellent agreement with the data is obtained when a relativistic scalar-vector kaon potential, that has stronger density dependence, is used. We further find that the transverse momentum dependence of directed and elliptic flow is quite sensitive to the kaon potential in dense matter.Comment: 5 pages, Revtex, 4 figure

    The pK0\Sigma+ final state in proton-proton collisions

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    This paper reports results from a study of the reaction pp->pK0\Sigma+ at beam momenta of p_{beam} = 2950, 3059, and 3200 MeV/c (excess energies of \epsilon= 126, 161, and 206 MeV). Total cross sections were determined for all energies; a set of differential cross sections (Dalitz plots; invariant mass spectra of all two-body subsystems; angular distributions of all final state particles; distributions in helicity and Jackson frames) are presented for \epsilon= 161 MeV. The total cross sections are proportional to the volume of available three-body phase-space indicating that the transition matrix element does not change significantly in this range of excess energies. It is concluded from the differential data that the reaction proceeds dominantly via the N(1710)P_{11} and/or N(1720)P_{13} resonance(s); N(1650)S_{11} and \Delta(1600)P_{33} could also contribute.Comment: 15 pages, 10 figure

    C19 Biomedical X-ray Imaging, Current Status and Some Future Challenges

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    The fine structure of bioreactor liver tissue seen through the eyes of X-ray micro-computed tomography

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    High-speed three-dimensional X-ray computed tomography: The dynamic spatial reconstructor

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    Structural morphology of renal vasculature

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    An automatic segmentation technique has been developed and applied to two renal micro-computer tomography (CT) images. With the use of a 20-microm voxel resolution image, the arterial and venous trees were segmented for the rat renal vasculature, distinguishing resolving vessels down to 30 microm in radius. A higher resolution 4-microm voxel image of a renal vascular subtree, with vessel radial values down to 10 microm, was segmented. Strahler ordering was applied to each subtree using an iterative scheme developed to integrate information from the two segmented models to reconstruct the complete topology of the entire vascular tree. An error analysis of the assigned orders quantified the robustness of the ordering process for the full model. Radial, length, and connectivity data of the complete arterial and venous trees are reported by order. Substantial parallelism is observed between individual arteries and veins, and the ratio of parallel vessel radii is quantified via a power law. A strong correlation with Murray's Law was established, providing convincing evidence of the \"minimum work\" hypothesis. Results were compared with theoretical branch angle formulations, based on the principles of \"minimum shear force,\" were inconclusive. Three-dimensional reconstructions of renal vascular trees collected are made freely available for further investigation into renal physiology and modeling studies

    Inhibition of Cdc25A Suppresses Hepato-Renal Cystogenesis in Rodent Models of Polycystic Kidney and Liver Disease

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    BACKGROUND & AIMS: In polycystic kidney (PKD) and liver (PLD) diseases, the normally non-proliferative hepato-renal epithelia acquire a proliferative, cystic phenotype, which is linked to overexpression of Cdc25A and cell cycle deregulation. We investigated the effects of Cdc25A inhibition in mice and rats, via genetic and pharmacological approaches. METHODS: Cdc25A(+/-) mice (which have reduced levels of Cdc25A) were cross-bred with Pkhd1(del2/del2) mice (which have increased levels of Cdc25A and develop hepatic cysts). Cdc25A expression was analyzed in livers of control and PCK rats, control and Pkd2(ws25/-) mice, healthy individuals, and patients with PLD. We examined effects of pharmacologic inhibition of Cdc25A with Vitamin K3 (VK3) on the cell cycle, proliferation, and cyst expansion in vitro; hepato-renal cystogenesis in PCK rats and Pkd2(ws25/-) mice; and expression of Cdc25A and the cell cycle proteins regulated by Cdc25A. We also examined effects of the Cdc25A inhibitor PM-20 on hepato-renal cystogenesis in Pkd2(ws25/-) mice. RESULTS: Liver weights and hepatic and fibrotic areas were decreased by 32%-52% in Cdc25A(+/-):Pkhd1(del2/del2) mice, compared to Pkhd1(del2/del2) mice.VK3 altered the cell cycle and reduced proliferation of cultured cholangiocytes by 32%-83% and decreased growth of cultured cysts by 23%-67%. In PCK rats and Pkd2(ws25/-) mice, VK3 reduced liver and kidney weights and hepato-renal cystic and fibrotic areas by 18%-34%. PM-20 decreased hepato-renal cystogenesis in Pkd2(ws25/-) mice by 15%. CONCLUSIONS: Cdc25A inhibitors block cell cycle progression and proliferation, reduce liver and kidney weights and cyst growth in animal models of PKD and PLD, and might be developed as therapeutics for these diseases
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