124 research outputs found

    Q-Value for the Fermi Beta-Decay of 46V

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    By comparing the Q-values for the 46Ti(3He,t)46V and 47Ti(3He,t)47}V reactions to the isobaric analog states the Q-value for the superallowed Fermi-decay of 46V has been determined as Q_{EC}(46V)=(7052.11+/-0.27) keV. The result is compatible with the values from two recent direct mass measurements but is at variance with the previously most precise reaction Q-value. As additional input quantity we have determined the neutron separation energy S_n(47Ti)=(8880.51+/-0.25) keV

    Level density of 56^{56}Fe and low-energy enhancement of γ\gamma-strength function

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    The 55^{55}Mn(d,n)56(d,n)^{56}Fe differential cross section is measured at Ed=7E_d=7 MeV\@. The 56^{56}Fe level density obtained from neutron evaporation spectra is compared to the level density extracted from the 57^{57}Fe(3(^3He,αγ)56\alpha\gamma)^{56}Fe reaction by the Oslo-type technique. Good agreement is found between the level densities determined by the two methods. With the level density function obtained from the neutron evaporation spectra, the 56^{56}Fe γ\gamma-strength function is also determined from the first-generation γ\gamma matrix of the Oslo experiment. The good agreement between the past and present results for the γ\gamma-strength function supports the validity of both methods and is consistent with the low-energy enhancement of the γ\gamma strength below 4\sim 4 MeV first discovered by the Oslo method in iron and molybdenum isotopes.Comment: 7 pages, 5 figure

    Combinatorial nuclear level density by a Monte Carlo method

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    We present a new combinatorial method for the calculation of the nuclear level density. It is based on a Monte Carlo technique, in order to avoid a direct counting procedure which is generally impracticable for high-A nuclei. The Monte Carlo simulation, making use of the Metropolis sampling scheme, allows a computationally fast estimate of the level density for many fermion systems in large shell model spaces. We emphasize the advantages of this Monte Carlo approach, particularly concerning the prediction of the spin and parity distributions of the excited states, and compare our results with those derived from a traditional combinatorial or a statistical method. Such a Monte Carlo technique seems very promising to determine accurate level densities in a large energy range for nuclear reaction calculations.Comment: 30 pages, LaTex, 7 figures (6 Postscript figures included). Fig. 6 upon request to the autho

    Study of the nucleon-induced preequilibrium reactions in terms of the Quantum Molecular Dynamics

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    The preequilibrium (nucleon-in, nucleon-out) angular distributions of 27^{27}Al, 58^{58}Ni and 90^{90}Zr have been analyzed in the energy region from 90 to 200 MeV in terms of the Quantum Moleculear Dynamics (QMD) theory. First, we show that the present approach can reproduce the measured (p,xp') and (p,xn) angular distributions leading to continuous final states without adjusing any parameters. Second, we show the results of the detailed study of the preequilibrium reaction processes; the step-wise contribution to the angular distribution, comparison with the quantum-mechanical Feshbach-Kerman-Koonin theory, the effects of momentum distribution and surface refraction/reflection to the quasifree scattering. Finally, the present method was used to assess the importance of multiple preequilibrium particle emission as a function of projectile energy up to 1 GeV.Comment: 22pages, Revex is used, 10 Postscript figures are available by request from [email protected]

    Endothelial-Mesenchymal Transition of Brain Endothelial Cells: Possible Role during Metastatic Extravasation

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    Cancer progression towards metastasis follows a defined sequence of events described as the metastatic cascade. For extravasation and transendothelial migration metastatic cells interact first with endothelial cells. Yet the role of endothelial cells during the process of metastasis formation and extravasation is still unclear, and the interaction between metastatic and endothelial cells during transendothelial migration is poorly understood. Since tumor cells are well known to express TGF-beta, and the compact endothelial layer undergoes a series of changes during metastatic extravasation (cell contact disruption, cytoskeletal reorganization, enhanced contractility), we hypothesized that an EndMT may be necessary for metastatic extravasation. We demonstrate that primary cultured rat brain endothelial cells (BEC) undergo EndMT upon TGF-beta 1 treatment, characterized by the loss of tight and adherens junction proteins, expression of fibronectin, beta 1-integrin, calponin and a-smooth muscle actin (SMA). B16/F10 cell line conditioned and activated medium (ACM) had similar effects: claudin-5 down-regulation, fibronectin and SMA expression. Inhibition of TGF-beta signaling during B16/F10 ACM stimulation using SB-431542 maintained claudin-5 levels and mitigated fibronectin and SMA expression. B16/F10 ACM stimulation of BECs led to phosphorylation of Smad2 and Smad3. SB-431542 prevented SMA up-regulation upon stimulation of BECs with A2058, MCF-7 and MDA-MB231 ACM as well. Moreover, B16/F10 ACM caused a reduction in trans-endothelial electrical resistance, enhanced the number of melanoma cells adhering to and transmigrating through the endothelial layer, in a TGF-beta-dependent manner. These effects were not confined to BECs: HUVECs showed TGF-beta-dependent SMA expression when stimulated with breast cancer cell line ACM. Our results indicate that an EndMT may be necessary for metastatic transendothelial migration, and this transition may be one of the potential mechanisms occurring during the complex phenomenon known as metastatic extravasation

    Multifactorial anticancer effects of digalloyl-resveratrol encompass apoptosis, cell-cycle arrest, and inhibition of lymphendothelial gap formation in vitro

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    BACKGROUND: Digalloyl-resveratrol (di-GA) is a synthetic compound aimed to combine the biological effects of the plant polyhydroxy phenols gallic acid and resveratrol, which are both radical scavengers and cyclooxygenase inhibitors exhibiting anticancer activity. Their broad spectrum of activities may probably be due to adjacent free hydroxyl groups. METHODS: Protein activation and expression were analysed by western blotting, deoxyribonucleoside triphosphate levels by HPLC, ribonucleotide reductase activity by 14 C-cytidine incorporation into nascent DNA and cell-cycle distribution by FACS. Apoptosis was measured by Hoechst 33258/propidium iodide double staining of nuclear chromatin and the formation of gaps into the lymphendothelial barrier in a three-dimensional co-culture model consisting of MCF-7 tumour cell spheroids and human lymphendothelial monolayers. RESULTS: In HL-60 leukaemia cells, di-GA activated caspase 3 and dose-dependently induced apoptosis. It further inhibited cell-cycle progression in the G1 phase by four different mechanisms: rapid downregulation of cyclin D1, induction of Chk2 with simultaneous downregulation of Cdc25A, induction of the Cdk-inhibitor p21(Cip/Waf) and inhibition of ribonucleotide reductase activity resulting in reduced dCTP and dTTP levels. Furthermore, di-GA inhibited the generation of lymphendothelial gaps by cancer cell spheroid-secreted lipoxygenase metabolites. Lymphendothelial gaps, adjacent to tumour bulks, can be considered as gates facilitating metastatic spread. CONCLUSION: These data show that di-GA exhibits three distinct anticancer activities: induction of apoptosis, cell-cycle arrest and disruption of cancer cell-induced lymphendothelial disintegration. British Journal of Cancer (2010) 102, 1361-1370. doi:10.1038/sj.bjc.6605656 www.bjcancer.com (C) 2010 Cancer Research U
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