Approaching the Intrinsic Bandgap in Suspended High-Mobility Graphene Nanoribbons

We report electrical transport measurements on a suspended ultra-low-disorder graphene nanoribbon(GNR) with nearly atomically smooth edges that reveal a high mobility exceeding 3000 cm2 V-1 s-1 and an intrinsic band gap. The experimentally derived bandgap is in quantitative agreement with the results of our electronic-structure calculations on chiral GNRs with comparable width taking into account the electron-electron interactions, indicating that the origin of the bandgap in non-armchair GNRs is partially due to the magnetic zigzag edges.Comment: 22 pages, 6 figure

Entanglement measurement based on two-particle interference

We propose a simple and realizable method using a two-particle interferometer for the experimental measurement of pairwise entanglement, assuming some prior knowledge about the quantum state. The basic idea is that the properties of the density matrix can be revealed by the single- and two-particle interference patterns. The scheme can easily be implemented with polarized entangled photons.Comment: 5 pages, 1 figur

Centrality, system size and energy dependences of charged-particle pseudo-rapidity distribution

Utilizing the three-fireball picture within the quark combination model, we study systematically the charged particle pseudorapidity distributions in both Au+Au and Cu+Cu collision systems as a function of collision centrality and energy, $\sqrt{s_{NN}}=$ 19.6, 62.4, 130 and 200 GeV, in full pseudorapidity range. We find that: (i)the contribution from leading particles to $dN_{ch}/d\eta$ distributions increases with the decrease of the collision centrality and energy respectively; (ii)the number of the leading particles is almost independent of the collision energy, but it does depend on the nucleon participants $N_{part}$; (iii)if Cu+Cu and Au+Au collisions at the same collision energy are selected to have the same $N_{part}$, the resulting of charged particle $dN/d\eta$ distributions are nearly identical, both in the mid-rapidity particle density and the width of the distribution. This is true for both 62.4 GeV and 200 GeV data. (iv)the limiting fragmentation phenomenon is reproduced. (iiv) we predict the total multiplicity and pseudorapidity distribution for the charged particles in Pb+Pb collisions at $\sqrt{s_{NN}}= 5.5$ TeV. Finally, we give a qualitative analysis of the $N_{ch}/$ and $dN_{ch}/d\eta/|_{\eta\approx0}$ as function of $\sqrt{s_{NN}}$ and $N_{part}$ from RHIC to LHC.Comment: 12 pages, 8 figure

A Multi-Phase Transport Model for Relativistic Heavy Ion Collisions

We describe in detail how the different components of a multi-phase transport (AMPT) model, that uses the Heavy Ion Jet Interaction Generator (HIJING) for generating the initial conditions, Zhang's Parton Cascade (ZPC) for modeling partonic scatterings, the Lund string fragmentation model or a quark coalescence model for hadronization, and A Relativistic Transport (ART) model for treating hadronic scatterings, are improved and combined to give a coherent description of the dynamics of relativistic heavy ion collisions. We also explain the way parameters in the model are determined, and discuss the sensitivity of predicted results to physical input in the model. Comparisons of these results to experimental data, mainly from heavy ion collisions at the Relativistic Heavy Ion Collider (RHIC), are then made in order to extract information on the properties of the hot dense matter formed in these collisions.Comment: 33 pages, 38 figures, revtex. Added 9 figures, version published in Phys. Rev. C. The full source code of the AMPT model in the Fortran 77 language and instructions for users are available from the EPAPS ftp site (ftp://ftp.aip.org/epaps/phys_rev_c/E-PRVCAN-72-781512/) and the OSCAR website (http://www-cunuke.phys.columbia.edu/OSCAR/

Nature of magnetotransport in metal/insulating-ferromagnet heterostructures: Spin Hall magnetoresistance or magnetic proximity effect

We study the anomalous Hall-like effect (AHLE) and the effective anisotropic magnetoresistance (EAMR) in antiferromagnetic {\gamma} -IrMn3/Y3Fe5O12(YIG) and Pt/YIG heterostructures. For {\gamma} -IrMn3/YIG, the EAMR and the AHLE resistivity change sign with temperature due to the competition between the spin Hall magnetoresistance (SMR) and the magnetic proximity effect (MPE) induced by the interfacial antiferromagnetic uncompensated magnetic moment. In contrast, for Pt/YIG the AHLE resistivity changes sign with temperature whereas no sign change is observed in the EAMR. This is because the MPE and the SMR play a dominant role in the AHLE and the EAMR, respectively. As new types of galvanomagnetic property, the AHLE and the EAMR have proved vital in disentangling the MPE and the SMR in metal/insulating-ferromagnet heterostructures

Multiple functional neurosteroid binding sites on GABAA receptors

Neurosteroids are endogenous modulators of neuronal excitability and nervous system development and are being developed as anesthetic agents and treatments for psychiatric diseases. While gamma amino-butyric acid Type A (GABAA) receptors are the primary molecular targets of neurosteroid action, the structural details of neurosteroid binding to these proteins remain ill defined. We synthesized neurosteroid analogue photolabeling reagents in which the photolabeling groups were placed at three positions around the neurosteroid ring structure, enabling identification of binding sites and mapping of neurosteroid orientation within these sites. Using middle-down mass spectrometry (MS), we identified three clusters of photolabeled residues representing three distinct neurosteroid binding sites in the human α1β3 GABAA receptor. Novel intrasubunit binding sites were identified within the transmembrane helical bundles of both the α1 (labeled residues α1-N408, Y415) and β3 (labeled residue β3-Y442) subunits, adjacent to the extracellular domains (ECDs). An intersubunit site (labeled residues β3-L294 and G308) in the interface between the β3(+) and α1(-) subunits of the GABAA receptor pentamer was also identified. Computational docking studies of neurosteroid to the three sites predicted critical residues contributing to neurosteroid interaction with the GABAA receptors. Electrophysiological studies of receptors with mutations based on these predictions (α1-V227W, N408A/Y411F, and Q242L) indicate that both the α1 intrasubunit and β3-α1 intersubunit sites are critical for neurosteroid action

RhoA/Rho Kinase Mediates Neuronal Death Through Regulating cPLA2 Activation

Activation of RhoA/Rho kinase leads to growth cone collapse and neurite retraction. Although RhoA/Rho kinase inhibition has been shown to improve axon regeneration, remyelination and functional recovery, its role in neuronal cell death remains unclear. To determine whether RhoA/Rho kinase played a role in neuronal death after injury, we investigated the relationship between RhoA/Rho kinase and cytosolic phospholipase A2 (cPLA2), a lipase that mediates inflammation and cell death, using an in vitro neuronal death model and an in vivo contusive spinal cord injury model performed at the 10th thoracic (T10) vertebral level. We found that co-administration of TNF-α and glutamate induced spinal neuron death, and activation of RhoA, Rho kinase and cPLA2. Inhibition of RhoA, Rho kinase and cPLA2 significantly reduced TNF-α/glutamate-induced cell death by 33, 52 and 43 %, respectively (p < 0.001). Inhibition of RhoA and Rho kinase also significantly downregulated cPLA2 activation by 66 and 60 %, respectively (p < 0.01). Furthermore, inhibition of RhoA and Rho kinase reduced the release of arachidonic acid, a downstream substrate of cPLA2. The immunofluorescence staining showed that ROCK1 or ROCK2, two isoforms of Rho kinase, was co-localized with cPLA2 in neuronal cytoplasm. Interestingly, co-immunoprecipitation (Co-IP) assay showed that ROCK1 or ROCK2 bonded directly with cPLA2 and phospho-cPLA2. When the Rho kinase inhibitor Y27632 was applied in mice with T10 contusion injury, it significantly decreased cPLA2 activation and expression and reduced injury-induced apoptosis at and close to the lesion site. Taken together, our results reveal a novel mechanism of RhoA/Rho kinase-mediated neuronal death through regulating cPLA2 activation