932 research outputs found

    Implications of a new light gauge boson for neutrino physics

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    We study the impact of light gauge bosons on neutrino physics. We show that they can explain the NuTeV anomaly and also escape the constraints from neutrino experiments if they are very weakly coupled and have a mass of a few GeV. Lighter gauge bosons with stronger couplings could explain both the NuTeV anomaly and the positive anomalous magnetic moment of the muon. However, in the simple model we consider in this paper (say a purely vectorial extra U(1) current), they appear to be in conflict with the precise measurements of \nu-e elastic scattering cross sections. The surprising agreement that we obtain between our naive model and the NuTeV anomaly for a Z' mass of a few GeV may be a coincidence. However, we think it is interesting enough to deserve attention and perhaps a more careful analysis, especially since a new light gauge boson is a very important ingredient for the Light Dark Matter scenario.Comment: 9 page

    Hyperspectral imaging with scanning near-field optical microscopy: applications in plasmonics

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    We present the realisation of near-field spectroscopic measurements with fibre-tip-based scanning near-field microscopy. It allows the simultaneous acquisition of near-field images in a broad spectral range (400 nm to 1000 nm), thus recovering local spectroscopic information. This technique is essential in order to understand the resonant interaction of light with nanostructured material as the far-field and nearfield spectral response can differ significantly, e.g., in the case of plasmonic nanostructures. Several example applications of hyperspectral near-field imaging are given for visualisation of Bloch modes in plasmonic crystals and plasmon-assisted transmission through a slit. © 2010 Optical Society of America

    Broadband and broadangle SPP antennas based on plasmonic crystals with linear chirp

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    Plasmonic technology relies on the coupling of light to surface electromagnetic modes on smooth or structured metal surfaces. While some applications utilise the resonant nature of surface polaritons, others require broadband characteristics. We demonstrate unidirectional and broadband plasmonic antennas with large acceptance angles based on chirped plasmonic gratings. Near-field optical measurements have been used to visualise the excitation of surface plasmon polaritons by such aperiodic structures. These weakly aperiodic plasmonic crystals allow the formation of a trapped rainbow-type effect in a two-dimensional geometry as surface polaritons of different frequencies are coherently excited in different locations over the plasmonic structure. Both the crystal's finite size and the finite lifetime of plasmonic states are crucial for the generation of broadband surface plasmon polaritons. This approach presents new opportunities for building unidirectional, broadband and broad-angle plasmonic couplers for sensing purposes, information processing, photovoltaic applications and shaping and manipulating ultrashort optical pulses. © 2012 Macmillan Publishers Limited. All rights reserved

    Chemical chaperone treatment reduces intracellular accumulation of mutant collagen IV and ameliorates the cellular phenotype of a COL4A2 mutation that causes haemorrhagic stroke

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    Haemorrhagic stroke accounts for approximately 20% of stroke cases and porencephaly is a clinical consequence of perinatal cerebral haemorrhaging. Here we report the identification of a novel dominant G702D mutation in the collagen domain of COL4A2 (collagen IV alpha chain 2) in a family displaying porencephaly with reduced penetrance. COL4A2 is the obligatory protein partner of COL4A1 but in contrast to most COL4A1 mutations, the COL4A2 mutation does not lead to eye or kidney disease. Analysis of dermal biopsies from patient and his unaffected father, who also carries the mutation, revealed that both display basement membrane (BM) defects. Intriguingly, defective collagen IV incorporation into the dermal BM was only observed in the patient and was associated with endoplasmic reticulum (ER) retention of COL4A2 in primary dermal fibroblasts. This intracellular accumulation led to ER-stress, unfolded protein response activation, reduced cell proliferation and increased apoptosis. Interestingly, absence of ER retention of COL4A2 and ER-stress in cells from the unaffected father indicate that accumulation and/or clearance of mutant COL4A2 from the ER may be a critical modifier for disease development. Our analysis also revealed that mutant collagen IV is degraded via the proteasome. Importantly, treatment of patient cells with a chemical chaperone decreased intracellular COL4A2, ER-stress and apoptosis, demonstrating that reducing intracellular collagen accumulation can ameliorate the cellular phenotype of COL4A2 mutations. Importantly, these data highlight that manipulation of chaperone levels, intracellular collagen accumulation and ER-stress are potential therapeutic options for collagen IV diseases including haemorrhagic stroke

    Comparison of Navier Stokes and Reduced Navier Stokes unsteady computation in a stenosis

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    Differential roles of p39Mos–Xp42Mpk1 cascade proteins on Raf1 phosphorylation and spindle morphogenesis in Xenopus oocytes

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    AbstractFully-grown G2-arrested Xenopus oocytes resume meiosis upon hormonal stimulation. Resumption of meiosis is characterized by germinal vesicle breakdown, chromosome condensation, and organization of a bipolar spindle. These cytological events are accompanied by activation of MPF and the p39Mos–MEK1–Xp42Mpk1–p90Rsk pathways. The latter cascade is activated upon p39Mos accumulation. Using U0126, a MEK1 inhibitor, and p39Mos antisense morpholino and phosphorothioate oligonucleotides, we have investigated the role of the members of the p39Mos–MEK1–Xp42Mpk1–p90Rsk in spindle morphogenesis. First, we have observed at a molecular level that prevention of p39Mos accumulation always led to MEK1 phosphorylation defects, even when meiosis was stimulated through the insulin Ras-dependent pathway. Moreover, we have observed that Raf1 phosphorylation that occurs during meiosis resumption was dependent upon the activity of MEK1 or Xp42Mpk1 but not p90Rsk. Second, inhibition of either p39Mos accumulation or MEK1 inhibition led to the formation of a cytoplasmic aster-like structure that was associated with condensed chromosomes. Spindle morphogenesis rescue experiments using constitutively active Rsk and purified murine Mos protein suggested that p39Mos or p90Rsk alone failed to promote meiotic spindle organization. Our results indicate that activation of the p39Mos–MEK1–Xp42Mpk1–p90Rsk pathway is required for bipolar organization of the meiotic spindle at the cortex

    Mutations in the PCNA-binding site of CDKN1C inhibit cell proliferation by impairing the entry into S phase

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    Abstract\ud \ud CDKN1C (also known as P57\ud \ud kip2\ud ) is a cyclin-dependent kinase inhibitor that functions as a negative regulator of cell proliferation through G1 phase cell cycle arrest. Recently, our group described gain-of-function mutations in the PCNA-binding site of CDKN1C that result in an undergrowth syndrome called IMAGe Syndrome (Intrauterine Growth Restriction, Metaphyseal dysplasia, Adrenal hypoplasia, and Genital anomalies), with life-threatening consequences. Loss-of-function mutations in CDKN1C have been identified in 5-10% of individuals with Beckwith-Wiedemann syndrome (BWS), an overgrowth disorder with features that are the opposite of IMAGe syndrome. Here, we investigate the effects of IMAGe-associated mutations on protein stability, cell cycle progression and cell proliferation. Mutations in the PCNA-binding site of CDKN1C significantly increase CDKN1C protein stability and prevent cell cycle progression into the S phase. Overexpression of either wild-type or BWS-mutant CDKN1C inhibited cell proliferation. However, the IMAGe-mutant CDKN1C protein decreased cell growth significantly more than both the wild-type or BWS protein. These findings bring new insights into the molecular events underlying IMAGe syndrome.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP process number 2012/09391-0
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