Ionization and acceleration of multiply charged gold ions in solid film irradiated by high intensity laser

In this paper, we present the mechanisms of ionization of a thin gold film irradiated by a high-intensity, short-pulse laser in the range of I=10²⁰⁻²² W/cm² and the associated acceleration of multiply charged gold ions. A numerical one-dimensional simulation using an extended particle-in-cell code, which includes atomic and collisional relaxation processes, indicates that two types of acceleration, hole-boring radiation pressure acceleration (RPA) and target normal sheath acceleration (TNSA), contribute to the generation of highly charged ions with kinetic energies on the order of 10 MeV/u. In each acceleration, a longitudinal electrostatic field excited by different mechanisms dominantly ionizes atoms to higher charge states and accelerates them to the vacuum region from the rear surface, which is opposite the front surface irradiated by the laser field. The field ionization process dominantly ionizes high energy ions to the high charge state, while a large number of ions with energy <1 MeV/u are ionized by an electron impact ionization process. In TNSA, a multiply charged ion generated at the rear surface is accelerated to the maximum energy although the ion with the highest charge state is generated at the front surface in RPA. However, the existence of contamination, such as water vapor, suppresses the ion energy of TNSA to less than that of RPA since the sheath field readily accelerates the protons and oxygen prior to the acceleration of the gold ions. Our derived theoretical scaling describes the maximum ion energy for each charge state in the cases with and without contamination using the relationship between the longitudinal electrostatic field profile near the rear surface and the classical tunnel field ionization model

Perturbation Study of the Conductance through an Interacting Region Connected to Multi-Mode Leads

We study the effects of electron correlation on transport through an interacting region connected to multi-mode leads based on the perturbation expansion with respect to the inter-electron interaction. At zero temperature the conductance defined in the Kubo formalism can be written in terms of a single-particle Green's function at the Fermi energy, and it can be mapped onto a transmission coefficient of the free quasiparticles described by an effective Hamiltonian. We apply this formulation to a two-dimensional Hubbard model of finite size connected to two noninteracting leads. We calculate the conductance in the electron-hole symmetric case using the order $U^2$ self-energy. The conductance shows several maximums in the $U$ dependence in some parameter regions of $t_y/t_x$, where $t_x$ ($t_y$) is the hopping matrix element in the $x$- ($y$-) directions. This is caused by the resonance occurring in some of the subbands, and is related with the $U$ dependence of the eigenvalues of the effective Hamiltonian.Comment: 17 pages, 12 figures, to be published in J.Phys.Soc.Jpn. 71(2002)No.

Electron Standing Wave Formation in Atomic Wires

Using the Landauer formulation of transport theory and tight binding models of the electronic structure, we study electron transport through atomic wires that form 1D constrictions between pairs of metallic nano-contacts. Our results are interpreted in terms of electron standing waves formed in the atomic wires due to interference of electron waves reflected at the ends of the atomic constrictions. We explore the influence of the chemistry of the atomic wire-metal contact interfaces on these standing waves and the associated transport resonances by considering two types of atomic wires: gold wires attached to gold contacts and carbon wires attached to gold contacts. We find that the conductance of the gold wires is roughly $1 G_0 = 2 e^2/h$ for the wire lengths studied, in agreement with experiments. By contrast, for the carbon wires the conductance is found to oscillate strongly as the number of atoms in the wire varies, the odd numbered chains being more conductive than the even numbered ones, in agreement with previous theoretical work that was based on a different model of the carbon wire and metal contacts.Comment: 14 pages, includes 6 figure

Ion acceleration from microstructured targets irradiated by high-intensity picosecond laser pulses

Structures on the front surface of thin foil targets for laser-driven ion acceleration have been proposed to increase the ion source maximum energy and conversion efficiency. While structures have been shown to significantly boost the proton acceleration from pulses of moderate-energy fluence, their performance on tightly focused and high-energy lasers remains unclear. Here, we report the results of laser-driven three-dimensional (3D)-printed microtube targets, focusing on their efficacy for ion acceleration. Using the high-contrast (∼1012) PHELIX laser (150J, 1021W/cm2), we studied the acceleration of ions from 1-μm-thick foils covered with micropillars or microtubes, which we compared with flat foils. The front-surface structures significantly increased the conversion efficiency from laser to light ions, with up to a factor of 5 higher proton number with respect to a flat target, albeit without an increase of the cutoff energy. An optimum diameter was found for the microtube targets. Our findings are supported by a systematic particle-in-cell modeling investigation of ion acceleration using 2D simulations with various structure dimensions. Simulations reproduce the experimental data with good agreement, including the observation of the optimum tube diameter, and reveal that the laser is shuttered by the plasma filling the tubes, explaining why the ion cutoff energy was not increased in this regime.Fil: Bailly Grandvaux, M.. University of California at San Diego; Estados UnidosFil: Kawahito, D.. University of California at San Diego; Estados UnidosFil: McGuffey, C.. University of California at San Diego; Estados UnidosFil: Strehlow, J.. University of California at San Diego; Estados UnidosFil: Edghill, B.. University of California at San Diego; Estados UnidosFil: Wei, M.S.. Laboratory For Laser Energetics; Estados UnidosFil: Alexander, N.. General Atomics; Estados UnidosFil: Haid, A.. General Atomics; Estados UnidosFil: Brabetz, C.. Helmholtzzentrum Für Schwerionenforschung; AlemaniaFil: Bagnoud, V.. Helmholtzzentrum Für Schwerionenforschung; AlemaniaFil: Hollinger, R.. State University of Colorado - Fort Collins; Estados UnidosFil: Capeluto, Maria Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Física de Buenos Aires. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Física de Buenos Aires; ArgentinaFil: Rocca, J.J.. State University of Colorado - Fort Collins; Estados UnidosFil: Beg, F.N.. University of California at San Diego; Estados Unido

Device Thrombogenicity Emulation: A Novel Method for Optimizing Mechanical Circulatory Support Device Thromboresistance

Mechanical circulatory support (MCS) devices provide both short and long term hemodynamic support for advanced heart failure patients. Unfortunately these devices remain plagued by thromboembolic complications associated with chronic platelet activation – mandating complex, lifelong anticoagulation therapy. To address the unmet need for enhancing the thromboresistance of these devices to extend their long term use, we developed a universal predictive methodology entitled Device Thrombogenicity Emulation (DTE) that facilitates optimizing the thrombogenic performance of any MCS device – ideally to a level that may obviate the need for mandatory anticoagulation

15-Deoxy-Δ12,14 Prostaglandin J2 Reduces the Formation of Atherosclerotic Lesions in Apolipoprotein E Knockout Mice

AIM: 15-deoxy-Δ¹²,¹⁴ prostaglandin J₂ (15d-PGJ₂) is a ligand of peroxisome proliferator-activated receptor γ (PPARγ) having diverse effects such as the differentiation of adipocytes and atherosclerotic lesion formation. 15d-PGJ₂ can also regulate the expression of inflammatory mediators on immune cells independent of PPARγ. We investigated the antiatherogenic effect of 15d-PGJ₂. METHODS: We fed apolipoprotein (apo) E-deficient female mice a Western-type diet from 8 to 16 wk of age and administered 1 mg/kg/day 15d-PGJ₂ intraperitoneally. We measured atherosclerotic lesions at the aortic root, and examined the expression of macrophage and inflammatory atherosclerotic molecules by immunohistochemical and real-time PCR in the lesion. RESULTS: Atherosclerotic lesion formation was reduced in apo E-null mice treated with 15d-PGJ₂, as compared to in the controls. Immunohistochemical and real-time PCR analyses showed that the expression of MCP-1, TNF-α, and MMP-9 in atherosclerotic lesions was significantly decreased in 15d-PGJ₂ treated mice. The 15d-PGJ₂ also reduced the expression of macrophages and RelA mRNA in atherosclerotic lesions. CONCLUSION: This is the first report 15d-PGJ₂, a natural PPARγ agonist, can improve atherosclerotic lesions in vivo. 15d-PGJ₂ may be a beneficial therapeutic agent for atherosclerosis

Influence of hypothermia on right atrial cardiomyocyte apoptosis in patients undergoing aortic valve replacement

BACKGROUND: There is increasing evidence that programmed cell death can be triggered during cardiopulmonary bypass (CPB) and may be involved in postoperative complications. The purpose of this study was to investigate whether apoptosis occurs during aortic valve surgery and whether modifying temperature during CPB has any influence on cardiomyocyte apoptotic death rate. METHODS: 20 patients undergoing elective aortic valve replacement for aortic stenosis were randomly assigned to either moderate hypothermic (ModHT group, n = 10, 28°C) or mild hypothermic (MiHT group, n = 10, 34°C) CPB. Myocardial samples were obtained from the right atrium before and after weaning from CPB. Specimens were examined for apoptosis by flow cytometry analysis of annexin V-propidium iodide (PI) and Fas death receptor staining. RESULTS: In the ModHT group, non apoptotic non necrotic cells (annexin negative, PI negative) decreased after CPB, while early apoptotic (annexin positive, PI negative) and late apoptotic or necrotic (PI positive) cells increased. In contrast, no change in the different cell populations was observed over time in the MiHT group. Fas expression rose after reperfusion in the ModHT group but not in MiHT patients, in which there was even a trend for a lower Fas staining after CPB (p = 0.08). In ModHT patients, a prolonged ischemic time tended to induce a higher increase of Fas (p = 0.061). CONCLUSION: Our data suggest that apoptosis signal cascade is activated at early stages during aortic valve replacement under ModHT CPB. This apoptosis induction can effectively be attenuated by a more normothermic procedure

Quasi-particle description for the transport through a small interacting system

We study effects of electron correlation on the transport through a small interacting system connected to reservoirs using an effective Hamiltonian which describes the free quasi-particles of a Fermi liquid. The effective Hamiltonian is defined microscopically with the value of the self-energy at $\omega=0$. Specifically, we apply the method to a Hubbard chain of finite size $N$ ($=1, 2, 3, ...$), and calculate the self-energy within the second order in $U$ in the electron-hole symmetric case. When the couplings between the chain and the reservoirs on the left and right are small, the conductance for even $N$ decreases with increasing $N$ showing a tendency toward a Mott-Hubbard insulator. This is caused by the off-diagonal element of the self-energy, and this behavior is qualitatively different from that in the special case examined in the previous work. We also study the effects of the asymmetry in the two couplings. While the perfect transmission due to the Kondo resonance occurs for any odd $N$ in the symmetric coupling, the conductance for odd $N$ decreases with increasing $N$ in the case of the asymmetric coupling.Comment: 27 pages, RevTeX, 14 figures, to be published in Phys. Rev.

PPARγ agonists inhibit growth and expansion of CD133+ brain tumour stem cells

Brain tumour stem cells (BTSCs) are a small population of cells that has self-renewal, transplantation, multidrug resistance and recurrence properties, thus remain novel therapeutic target for brain tumour. Recent studies have shown that peroxisome proliferator-activated receptor gamma (PPARγ) agonists induce growth arrest and apoptosis in glioblastoma cells, but their effects on BTSCs are largely unknown. In this study, we generated gliospheres with more than 50% CD133+ BTSC by culturing U87MG and T98G human glioblastoma cells with epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF). In vitro treatment with PPARγ agonist, 15-Deoxy-Δ12,14-Prostaglandin J2 (15d-PGJ2) or all-trans retinoic acid resulted in a reversible inhibition of gliosphere formation in culture. Peroxisome proliferator-activated receptor gamma agonists inhibited the proliferation and expansion of glioma and gliosphere cells in a dose-dependent manner. Peroxisome proliferator-activated receptor gamma agonists also induced cell cycle arrest and apoptosis in association with the inhibition of EGF/bFGF signalling through Tyk2-Stat3 pathway and expression of PPARγ in gliosphere cells. These findings demonstrate that PPARγ agonists regulate growth and expansion of BTSCs and extend their use to target BTSCs in the treatment of brain tumour

PPARγ agonists inhibit growth and expansion of CD133+ brain tumour stem cells

Brain tumour stem cells (BTSCs) are a small population of cells that has self-renewal, transplantation, multidrug resistance and recurrence properties, thus remain novel therapeutic target for brain tumour. Recent studies have shown that peroxisome proliferator-activated receptor gamma (PPARγ) agonists induce growth arrest and apoptosis in glioblastoma cells, but their effects on BTSCs are largely unknown. In this study, we generated gliospheres with more than 50% CD133+ BTSC by culturing U87MG and T98G human glioblastoma cells with epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF). In vitro treatment with PPARγ agonist, 15-Deoxy-Δ12,14-Prostaglandin J2 (15d-PGJ2) or all-trans retinoic acid resulted in a reversible inhibition of gliosphere formation in culture. Peroxisome proliferator-activated receptor gamma agonists inhibited the proliferation and expansion of glioma and gliosphere cells in a dose-dependent manner. Peroxisome proliferator-activated receptor gamma agonists also induced cell cycle arrest and apoptosis in association with the inhibition of EGF/bFGF signalling through Tyk2-Stat3 pathway and expression of PPARγ in gliosphere cells. These findings demonstrate that PPARγ agonists regulate growth and expansion of BTSCs and extend their use to target BTSCs in the treatment of brain tumour