Anisotropy and periodicity in the density distribution of electrons in a quantum-well

We use low temperature near-field optical spectroscopy to image the electron density distribution in the plane of a high mobility GaAs quantum well. We find that the electrons are not randomly distributed in the plane, but rather form narrow stripes (width smaller than 150 nm) of higher electron density. The stripes are oriented along the [1-10 ] crystal direction, and are arranged in a quasi-periodic structure. We show that elongated structural mounds, which are intrinsic to molecular beam epitaxy, are responsible for the creation of this electron density texture.Comment: 10 pages, 3 figure

Near-field spectroscopy of a gated electron gas: a direct evidence for electrons localization

The near-field photoluminescence of a gated two-dimensional electron gas is measured. We use the negatively charged exciton, formed by binding of an electron to a photo-excited electron-hole pair, as an indicator for the local presence of charge. Large spatial fluctuations in the luminescence intensity of the negatively charged exciton are observed. These fluctuations are shown to be due to electrons localized in the random potential of the remote ionized donors. We use these fluctuations to image the electrons and donors distribution in the plane.Comment: 10 pages, 5 figures, to be published in PR

Theory of neutral and charged exciton scattering with electrons in semiconductor quantum wells

Electron scattering on both neutral ($X$) and charged ($X^-$) excitons in quantum wells is studied theoretically. A microscopic model is presented, taking into account both elastic and dissociating scattering. The model is based on calculating the exciton-electron direct and exchange interaction matrix elements, from which we derive the exciton scattering rates. We find that for an electron density of $10^9 {\rm cm}^{-2}$ in a GaAs QW at $T=5K$, the $X^-$ linewidth due to electron scattering is roughly twice as large as that of the neutral exciton. This reflects both the $X^-$ larger interaction matrix elements compared with those of $X$, and their different dependence on the transferred momentum. Calculated reflection spectra can then be obtained by considering the three electronic excitations of the system, namely, the heavy-hole and light-hole 1S neutral excitons, and the heavy-hole 1S charged exciton, with the appropriate oscillator strengths.Comment: 18 pages, 12 figure

Spin-Atomic Vibration Interaction and Spin-Flip Hamiltonian of a Single Atomic Spin in a Crystal Field

We derive the spin-atomic vibration interaction $V_{\rm SA}$ and the spin-flip Hamiltonian $V_{\rm SF}$ of a single atomic spin in a crystal field. We here apply the perturbation theory to a model with the spin-orbit interaction and the kinetic and potential energies of electrons. The model also takes into account the difference in vibration displacement between an effective nucleus and electrons, \Delta {{\boldmath r}}. Examining the coefficients of $V_{\rm SA}$ and $V_{\rm SF}$, we first show that $V_{\rm SA}$ appears for \Delta {{\boldmath r}}$\ne$0, while $V_{\rm SF}$ is present independently of \Delta {{\boldmath r}}. As an application, we next obtain $V_{\rm SA}$ and $V_{\rm SF}$ of an Fe ion in a crystal field of tetragonal symmetry. It is found that the magnitudes of the coefficients of $V_{\rm SA}$ can be larger than those of the conventional spin-phonon interaction depending on vibration frequency. In addition, transition probabilities per unit time due to $V_{\rm SA}$ and $V_{\rm SF}$ are investigated for the Fe ion with an anisotropy energy of $-|D|S_Z^2$, where $D$ is an anisotropy constant and $S_Z$ is the $Z$ component of a spin operator.Comment: 55 pages, 17 figures, to be published in J. Phys. Soc. Jpn. 79 (2010) No. 11, typos correcte

Validation of a chloroquine-induced cell death mechanism for clinical use against malaria

An alternative antimalarial pathway of an ‘outdated’ drug, chloroquine (CQ), may facilitate its return to the shrinking list of effective antimalarials. Conventionally, CQ is believed to interfere with hemozoin formation at nanomolar concentrations, but resistant parasites are able to efflux this drug from the digestive vacuole (DV). However, we show that the DV membrane of both resistant and sensitive laboratory and field parasites is compromised after exposure to micromolar concentrations of CQ, leading to an extrusion of DV proteases. Furthermore, only a short period of exposure is required to compromise the viability of late-stage parasites. To study the feasibility of this strategy, mice malaria models were used to demonstrate that high doses of CQ also triggered DV permeabilization in vivo and reduced reinvasion efficiency. We suggest that a time-release oral formulation of CQ may sustain elevated blood CQ levels sufficiently to clear even CQ-resistant parasites

Giant Phonon-induced Conductance in Scanning Tunneling Spectroscopy of Gate-tunable Graphene

The honeycomb lattice of graphene is a unique two-dimensional (2D) system where the quantum mechanics of electrons is equivalent to that of relativistic Dirac fermions. Novel nanometer-scale behavior in this material, including electronic scattering, spin-based phenomena, and collective excitations, is predicted to be sensitive to charge carrier density. In order to probe local, carrier-density dependent properties in graphene we have performed atomically-resolved scanning tunneling spectroscopy measurements on mechanically cleaved graphene flake devices equipped with tunable back-gate electrodes. We observe an unexpected gap-like feature in the graphene tunneling spectrum which remains pinned to the Fermi level (E_F) regardless of graphene electron density. This gap is found to arise from a suppression of electronic tunneling to graphene states near E_F and a simultaneous giant enhancement of electronic tunneling at higher energies due to a phonon-mediated inelastic channel. Phonons thus act as a "floodgate" that controls the flow of tunneling electrons in graphene. This work reveals important new tunneling processes in gate-tunable graphitic layers

CXCL10 Can Inhibit Endothelial Cell Proliferation Independently of CXCR3

CXCL10 (or Interferon-inducible protein of 10 kDa, IP-10) is an interferon-inducible chemokine with potent chemotactic activity on activated effector T cells and other leukocytes expressing its high affinity G protein-coupled receptor CXCR3. CXCL10 is also active on other cell types, including endothelial cells and fibroblasts. The mechanisms through which CXCL10 mediates its effects on non-leukocytes is not fully understood. In this study, we focus on the anti-proliferative effect of CXCL10 on endothelial cells, and demonstrate that CXCL10 can inhibit endothelial cell proliferation in vitro independently of CXCR3. Four main findings support this conclusion. First, primary mouse endothelial cells isolated from CXCR3-deficient mice were inhibited by CXCL10 as efficiently as wildtype endothelial cells. We also note that the proposed alternative splice form CXCR3-B, which is thought to mediate CXCL10's angiostatic activity, does not exist in mice based on published mouse CXCR3 genomic sequences as an in-frame stop codon would terminate the proposed CXCR3-B splice variant in mice. Second, we demonstrate that human umbilical vein endothelial cells and human lung microvascular endothelial cells that were inhibited by CXL10 did not express CXCR3 by FACS analysis. Third, two different neutralizing CXCR3 antibodies did not inhibit the anti-proliferative effect of CXCL10. Finally, fourth, utilizing a panel of CXCL10 mutants, we show that the ability to inhibit endothelial cell proliferation correlates with CXCL10's glycosaminoglycan binding affinity and not with its CXCR3 binding and signaling. Thus, using a very defined system, we show that CXCL10 can inhibit endothelial cell proliferation through a CXCR3-independent mechanism

FGFR4 Arg388 allele correlates with tumour thickness and FGFR4 protein expression with survival of melanoma patients

A single nucleotide polymorphism in the gene for FGFR4 (−Arg388) has been associated with progression in various types of human cancer. Although fibroblast growth factors (FGFs) belong to the most important growth factors in melanoma, expression of FGF receptor subtype 4 has not been investigated yet. In this study, the protein expression of this receptor was analysed in 137 melanoma tissues of different progression stages by immunohistochemistry. FGFR4 protein was expressed in 45% of the specimens and correlated with pTNM tumour stages (UICC, P=0.023 and AJCC, P=0.046), presence of microulceration (P=0.009), tumour vascularity (P=0.001), metastases (P=0.025), number of primary tumours (P=0.022), overall survival (P=0.047) and disease-free survival (P=0.024). Furthermore, FGFR4 Arg388 polymorphism was analysed in 185 melanoma patients by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The Arg388 allele was detected in 45% of the melanoma patients and was significantly associated with tumour thickness (by Clark's level of invasion (P=0.004) and by Breslow in mm (P=0.02)) and the tumour subtype nodular melanoma (P=0.002). However, there was no correlation of the FGFR4 Arg388 allele with overall and disease-free survival. In conclusion, the Arg388 genotype and the protein expression of FGFR4 may be potential markers for progression of melanoma