999 resultados para beta( ) delayed proton decay
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The energy of the vh9/2 orbital in nuclei above N = 82 drops rapidly in energy relative to the vf7/2 orbital as the occupancy of the πh11/2 orbital increases. These two neutron orbitals become nearly degenerate as the proton drip line is approached. In this work, we have discovered the new nuclides 161Os and 157W, and studied the decays of the proton emitter 160Re in detail. The 161Os and 160Re nuclei were produced in reactions of 290, 300 and 310 MeV 58Ni ions with an isotopically enriched 106Cd target, separated in‐flight using the RITU separator and implanted into the GREAT spectrometer. The 161Os α a decays populated the new nuclide 157W, which decayed by β‐particle emission. The β decay fed the known α‐decaying 1/2+ and 11/2− states in 157Ta, which is consistent with a vf7/2 ground state in 157W. The measured α‐decay energy and half‐life for 161Os correspond to a reduced α‐decay width that is compatible with s‐wave α‐particle emission, implying that its ground state is also a vf7/2 state. Over 7000 160Re nuclei were produced and the γ decays of a new isomeric state feeding the πd3/2 level in 160Re were discovered, but no evidence for the proton or a decay of the expected πh11/2 state could be found. The isomer decays offer a natural explanation for this non‐observation and provides a striking example of the influence of the near degeneracy of the vh9/2 and vf7/2 orbitals on the properties of nuclei in this region.
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Carpenter syndrome, a rare autosomal recessive disorder characterized by a combination of craniosynostosis, polysyndactyly, obesity, and other congenital malformations, is caused by mutations in RAB23, encoding a member of the Rab-family of small GTPases. In 15 out of 16 families previously reported, the disease was caused by homozygosity for truncating mutations, and currently only a single missense mutation has been identified in a compound heterozygote. Here, we describe a further 8 independent families comprising 10 affected individuals with Carpenter syndrome, who were positive for mutations in RAB23. We report the first homozygous missense mutation and in-frame deletion, highlighting key residues for RAB23 function, as well as the first splice-site mutation. Multi-suture craniosynostosis and polysyndactyly have been present in all patients described to date, and abnormal external genitalia have been universal in boys. High birth weight was not evident in the current group of patients, but further evidence for laterality defects is reported. No genotype-phenotype correlations are apparent. We provide experimental evidence that transcripts encoding truncating mutations are subject to nonsense-mediated decay, and that this plays an important role in the pathogenesis of many RAB23 mutations. These observations refine the phenotypic spectrum of Carpenter syndrome and offer new insights into molecular pathogenesis. (C) 2011 Wiley-Liss, Inc.
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Symptoms evoked by Thalassophryne nattereri fish envenomation include local oedema, severe pain and intense necrosis with strikingly inefficient healing, continuing for several weeks or months. Investigations carried out in our laboratory showed that, in the venom-induced acute inflammation, thrombosis in venules and constrictions in arterioles were highly visible, in contrast to a notable lack of inflammatory cell. Nevertheless, the reason that the venom toxins favour delayed local inflammatory response is poorly defined. In this study, we analysed the movement of leucocytes after T. nattereri venom injection in the intraplantar region of Swiss mice, the production of pro-inflammatory mediators and the venom potential to elicit matrix metalloproteinase production and extracellular matrix degradation. Total absence of mononuclear and neutrophil influx was observed until 14 days, but the venom stimulates pro-inflammatory mediator secretion. Matrix metalloproteinases (MMP)-2 and MMP-9 were detected in greater quantities, accompanied by tissue degradation of collagenous fibre. An influx of mononuclear cells was noted very late and at this time the levels of IL-6, IL-1 beta and MMP-2 remained high. Additionally, the action of venom on the cytoskeletal organization was assessed in vitro. Swift F-actin disruption and subsequent loss of focal adhesion was noted. Collectively these findings show that the altered specific interaction cell-matrix during the inflammatory process creates an inadequate environment for infiltration of inflammatory cells.
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The intermediacy of the geminate base proton pair (A*center dot center dot center dot H(+)) in excited-state proton-transfer (ESPT) reactions (two-step mechanism) has been investigated employing the synthetic flavylium salt 7-hydroxy-4-methyl-flavylium chloride (HMF). In aqueous solution, the ESPT mechanism involves solely the excited acid AH* and base A* forms of HMF as indicated by the fluorescence spectra and double-exponential fluorescence decays (two species, two decay times). However, upon addition of either 1,4-dioxane or 1,2-propylene glycol, the decays become triple-exponential with a term consistent with the presence of the geminate base proton pair A*center dot center dot center dot H(+). The geminate pair becomes detectable because of the increase in the recombination rate constant, k(rec), of (A*center dot center dot center dot H(+)) with increasing the mole fraction of added organic cosolvent. Because the two-step ESPT mechanism splits the intrinsic prototropic reaction rates (deprotonation of AH(+)*, k(d), and recombination, k(rec) of A*center dot center dot center dot H(+)) from the diffusion controlled rates (dissociation, k(diss) and formation, k(diff)[H(+)], of A*center dot center dot center dot H+), the experimental detection of the geminate pair provides a wealth of information on the proton-transfer reaction (k(d) and k(rec)) as well as on proton diffusion/migration (k(diss) and k(diff)).
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Coupled bone turnover is directed by the expression of receptor-activated NF-kappa B ligand (RANKL) and its decoy receptor, osteoprotegerin (OPG). Proinflammatory cytokines, such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) induce RANKL expression in bone marrow stromal cells. Here, we report that IL-1 beta and TNF-alpha-induced RANKL requires p38 mitogen-activating protein kinase (MAPK) pathway activation for maximal expression. Real-time PCR was used to assess the p38 contribution toward IL-1 beta and TNF-alpha-induced RANKL mRNA expression. Steady-state RANKL RNA levels were increased approximately 17-fold by IL-1 beta treatment and subsequently reduced similar to 70%-90% when p38 MAPK was inhibited with SB203580. RANKL mRNA stability data indicated that p38 MAPK did not alter the rate of mRNA decay in IL-1 beta-induced cells. Using a RANKL-luciferase cell line receptor containing a 120-kB segment of the 5' flanking region of the RANKL gene, reporter expression was stimulated 4-5-fold by IL-1 beta or TNF-alpha treatment. IL-1 beta-induced RANKL reporter expression was completely blocked with specific p38 inhibitors as well as dominant negative mutant constructs of MAPK kinase-3 and -6. In addition, blocking p38 signaling in bone marrow stromal cells partially inhibited IL-1 beta and TNF-alpha-induced osteoclastogenesis in vitro. Results from these studies indicate that p38 MAPK is a major signaling pathway involved in IL-1 beta and TNF-alpha-induced RANKL expression in bone marrow stromal cells.
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We discuss the decay of accelerated protons and illustrate how the Fulling-Davies-Unruh effect is indeed mandatory to maintain the consistency of standard Quantum Field Theory. The confidence level of the Fulling-Davies-Unruh effect must be the same as that of Quantum Field Theory itself.
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A measurement of the top quark pair production cross section in proton antiproton collisions at an interaction energy of root s=1.96 TeV is presented. This analysis uses 405 +/- 25 pb(-1) of data collected with the D0 detector at the Fermilab Tevatron Collider. Fully hadronic t (t) over bar decays with final states of six or more jets are separated from the multijet background using secondary vertex tagging and a neural network. The t (t) over bar cross section is measured as sigma(t (t) over bar)=4.5(-1.9)(+2.0)(stat)(-1.1)(+1.4)(syst)+/- 0.3(lumi) pb for a top quark mass of m(t)=175 GeV/c(2).
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We measure the dimuon charge asymmetry A in p (p) over bar collisions at a center of mass energy root s=1960 GeV. The data was recorded with the D0 detector and corresponds to an integrated luminosity of approximately 1.0 fb(-1). Assuming that the asymmetry A is due to asymmetric B-0 <->(B) over bar (0) mixing and decay, we extract the CP-violation parameter of B-0 mixing and decay: ((epsilon B0))/(1+vertical bar epsilon B0 vertical bar 2)=(AB0)/(4)= -0.0023 +/- 0.0011(stat)+/- 0.0008(syst).A(B)(0) is the dimuon charge asymmetry from decays of B-0(B) over bar (0) pairs. The general case, with CP violation in both B-0 and B-s(0) systems, is also considered. Finally we obtain the forward-backward asymmetry that quantifies the tendency of mu(+) to go in the proton direction and mu(-) to go in the antiproton direction. The results are consistent with the standard model and constrain new physics.
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We make a careful study about the nonrelativistic reduction of one-meson-exchange models for the nonmesonic weak hypernuclear decay. Starting from a widely accepted effective coupling Hamiltonian involving the exchange of the complete pseudoscalar and vector meson octets (pi, eta, K, rho, omega, K*), the strangeness-changing weak LambdaN --> NN transition potential is derived, including two effects that have been systematically omitted in the literature, or, at best, only partly considered. These are the kinematical effects due to the difference between the lambda and nucleon masses, and the first-order nonlocality corrections, i.e., those involving up to first-order differential operators. Our analysis clearly shows that the main kinematical effect on the local contributions is the reduction of the effective pion mass. The kinematical effect on the nonlocal contributions is more complicated, since it activates several new terms that would otherwise remain dormant. Numerical results for C-12(Lambda) and He-5(Lambda) are presented and they show that the combined kinematical plus nonlocal corrections have an appreciable influence on the partial decay rates. However, this is somewhat diminished in the main decay observables: the total nonmesonic rate, Gamma(nm), the neutron-to-proton branching ratio, Gamma(n)/Gamma(p), and the asymmetry parameter, a(Lambda). The latter two still cannot be reconciled with the available experimental data. The existing theoretical predictions for the sign of a(Lambda) in He-5(Lambda) are confirmed. (C) 2003 Elsevier B.V. All rights reserved.
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)