123 research outputs found

    Collisionless shock acceleration of narrow energy spread ion beams from mixed species plasmas using 1 μ\mum lasers

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    Collisionless shock acceleration of protons and C6+^{6+} ions has been achieved by the interaction of a 1020^{20} W/cm2^2, 1 μ\mum laser with a near-critical density plasma. Ablation of the initially solid density target by a secondary laser allowed for systematic control of the plasma profile. This enabled the production of beams with peaked spectra with energies of 10-18 MeV/a.m.u. and energy spreads of 10-20%\% with up to 3x109^9 particles within these narrow spectral features. The narrow energy spread and similar velocity of ion species with different charge-to-mass ratio are consistent with acceleration by the moving potential of a shock wave. Particle-in-cell simulations show shock accelerated beams of protons and C6+^{6+} ions with energy distributions consistent with the experiments. Simulations further indicate the plasma profile determines the trade-off between the beam charge and energy and that with additional target optimization narrow energy spread beams exceeding 100 MeV/a.m.u. can be produced using the same laser conditions.Comment: Accepted for publication in Physical Review Accelerators and Beam

    Optimization of plasma amplifiers

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    Plasma amplifiers offer a route to side-step limitations on chirped pulse amplification and generate laser pulses at the power frontier. They compress long pulses by transferring energy to a shorter pulse via the Raman or Brillouin instabilities. We present an extensive kinetic numerical study of the three-dimensional parameter space for the Raman case. Further particle-in-cell simulations find the optimal seed pulse parameters for experimentally relevant constraints. The high-efficiency self-similar behavior is observed only for seeds shorter than the linear Raman growth time. A test case similar to an upcoming experiment at the Laboratory for Laser Energetics is found to maintain good transverse coherence and high-energy efficiency. Effective compression of a 10 kJ , nanosecond-long driver pulse is also demonstrated in a 15-cm-long amplifier

    Innervation Changes Induced by Inflammation in the Murine Vagina

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    © 2018 IBRO. Published by Elsevier Ltd. This manuscript version is made available under the CC-BY-NC-ND 4.0 license: http://creativecommons.org/licenses/by-nc-nd/4.0/ This author accepted manuscript is made available following 12 month embargo from date of publication (January 2018) in accordance with the publisher’s archiving policyVulvodynia is a prevalent chronic pain disorder associated with high medical costs and often ineffective treatments. The major pathological feature is proliferation of vaginal nerve fibers. This study aimed to develop a highly reproducible animal model to study neuroproliferation in the vagina and aid the identification of appropriately targeted treatments for conditions such as vulvodynia. Mild chronic inflammation was induced using microinjection of complete Freund’s adjuvant in the distal vagina of C57Bl/6 mice. Control mice received saline. Inflammation and innervation density were assessed at 7 and 28 days after a single administration or 14 days following repeated administration of complete Freund’s adjuvant or saline. Histochemistry and blinded-analysis of images were used to assess vaginal morphology (H & E) and abundance of macrophages (CD68-labeling), mast cells (toluidine blue staining, mast cell tryptase-immunoreactivity), blood vessels (αSMA-immunoreactivity) and nerve fibers immunoreactive for the pan-neuronal marker PGP9.5. Subpopulations of nerve fibers were identified using immunoreactivity for calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY). Single administration of complete Freund’s adjuvant resulted in vaginal swelling, macrophage infiltration, vascular proliferation and increased abundance of nerve fibers immunoreactive for CGRP, SP, VIP and/or PGP9.5 but not NPY, evident at seven days. Inflammation further increased following repeated administration of complete Freund’s adjuvant but nerve fiber proliferation did not. Nerve fiber proliferation continued to be evident at 28 days. The inter-individual differences within each treatment group were small, indicating that this model may be useful to study mechanisms underlying vaginal nerve fiber proliferation associated with inflammation

    Catalytic stereoselective addition to alkynes. Borylation or silylation promoted by magnesia-supported iron oxide and cis-diboronation or silaboration by supported platinum nanoparticles

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    Iron oxide nanoparticles supported on magnesia (FeO/MgO) have been prepared by NaBH4 reduction of Fe(SO4) on MgO and spontaneous reoxidation upon storage. XPS of FeO/MgO indicates the presence of Fe(0) (16%) and Fe(II) (84%) on this solid. TEM images show that catalytically active FeO/MgO is constituted by iron oxide nanoparticles of about 25 nm dispersed on fibrous MgO. FeO/MgO in the presence of catalytic amounts of triphenylphosphine promotes highly regio- and stereoselective monoborylation of aromatic, aliphatic, terminal and internal alkynes. Chemical analysis of the liquid after the reaction and control experiments using Fe(II) salts in the absence or presence of PPh3 supports that catalysis is heterogeneous. The possibility that trace amounts of copper impurities present in the iron precursor influence the catalytic activity of FeO/MgO was studied using a commercially available high-purity Fe(SO4) as precursor (99.999% Fe purity) showing again good (but lower) activity. In addition, a control experiment using as catalyst MgO containing 30 times higher amounts of Cu than that present in low purity Fe did not lead to complete alkyne conversion, although product formation was observed in a large extent. Alkynes react with complete chemoselectivity versus alkenes. In contrast to FeO/MgO, Pt supported on MgO or active carbon efficiently promotes the stereoselective diboronation and silaboration of alkynes in the absence of triphenylphosphine at lower temperature to render the cis configured diboronated and silaborated alkene.Financial support by the Spanish Ministry of the Economy and Competitiveness (Severo Ochoa and CTQ2012-32315) and the Generalidad Valenciana (Prometeo 2012-014) is gratefully acknowledged. This work was also funded by the Deanship of Scientific Research (DSR), King Abdulaziz University under grant No. 75-130-35-HiCi. The authors, therefore, acknowledge technical and financial support of KAU.Khan, A.; Asiri, AM.; Kosa, SA.; García Gómez, H.; Grirrane, A. (2015). Catalytic stereoselective addition to alkynes. Borylation or silylation promoted by magnesia-supported iron oxide and cis-diboronation or silaboration by supported platinum nanoparticles. Journal of Catalysis. 329:401-412. https://doi.org/10.1016/j.jcat.2015.05.006S40141232

    Genetic Evidence for Involvement of Neuronally Expressed S1P1 Receptor in Nociceptor Sensitization and Inflammatory Pain

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    Sphingosine-1-phosphate (S1P) is a key regulator of immune response. Immune cells, epithelia and blood cells generate high levels of S1P in inflamed tissue. However, it is not known if S1P acts on the endings of nociceptive neurons, thereby contributing to the generation of inflammatory pain. We found that the S1P1 receptor for S1P is expressed in subpopulations of sensory neurons including nociceptors. Both S1P and agonists at the S1P1 receptor induced hypersensitivity to noxious thermal stimulation in vitro and in vivo. S1P-induced hypersensitivity was strongly attenuated in mice lacking TRPV1 channels. S1P and inflammation-induced hypersensitivity was significantly reduced in mice with a conditional nociceptor-specific deletion of the S1P1 receptor. Our data show that neuronally expressed S1P1 receptors play a significant role in regulating nociceptor function and that S1P/S1P1 signaling may be a key player in the onset of thermal hypersensitivity and hyperalgesia associated with inflammation

    Modulation of the Akt/Ras/Raf/MEK/ERK pathway by A3 adenosine receptor

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    Downstream A3 receptor signalling plays an important role in the regulation of cell death and proliferation. Therefore, it is important to determine the molecular pathways involved through A3 receptor stimulation. The phosphatidylinositide-3-OH kinase (PI3K)/Akt and the Raf/mitogen-activated protein kinase (MAPK/ERK) kinase (MEK)/mitogen-activated protein kinase (MAPK) pathways have central roles in the regulation of cell survival and proliferation. The crosstalk between these two pathways has also been investigated. The focus of this review centres on downstream mediators of A3 adenosine receptor signalling
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