Weak Localization and Antilocalization in Topological Insulator Thin Films with Coherent Bulk-Surface Coupling

We evaluate quantum corrections to conductivity in an electrically gated thin film of a three-dimensional (3D) topological insulator (TI). We derive approximate analytical expressions for the low-field magnetoresistance as a function of bulk doping and bulk-surface tunneling rate. Our results reveal parameter regimes for both weak localization and weak antilocalization, and include diffusive Weyl semimetals as a special case.Comment: After publication, we have noticed and corrected two small but potentially misleading typographic errors in Eqs. (2.27) and (2.29), where the definitions of \tau_s and \tau_v were mistakenly switched. Once these typographic errors are fixed, all the results remain unchanged. An Erratum will be published in PR

Interplay between Symmetric Exchange Anisotropy, Uniform Dzyaloshinskii-Moriya Interaction and Magnetic Fields in the Phase Diagram of Quantum Magnets and Superconductors

We theoretically study the joint influence of uniform Dzyaloshinskii-Moriya (DM) interactions, symmetric exchange anisotropy (with its axis parallel to the DM vector) and arbitrarily oriented magnetic fields on one-dimensional spin 1/2 antiferromagnets. We show that the zero-temperature phase diagram contains three competing phases: (i) an antiferromagnet with Neel vector in the plane spanned by the DM vector and the magnetic field, (ii) a {\em dimerized} antiferromagnet with Neel vector perpendicular to both the DM vector and the magnetic field, and (iii) a gapless Luttinger liquid. Phase (i) is destroyed by a small magnetic field component along the DM vector and is furthermore unstable beyond a critical value of easy-plane anisotropy, which we estimate using Abelian and non-Abelian bosonization along with perturbative renormalization group. We propose a mathematical equivalent of the spin model in a one-dimensional Josephson junction (JJ) array located in proximity to a bulk superconductor. We discuss the analogues of the magnetic phases in the superconducting context and comment on their experimental viability.Comment: 20 pages, 16 figures; submitted to Phys. Rev.

Development of thermally formed glass optics for astronomical hard x-ray telescopes

The next major observational advance in hard X-ray/soft gamma-ray astrophysics will come with the implementation of telescopes capable of focusing 10-200 keV radiation. Focusing allows high signal-to-noise imaging and spectroscopic observations of many sources in this band for the first time. The recent development of depth-graded multilayer coatings has made the design of telescopes for this bandpass practical, however the ability to manufacture inexpensive substrates with appropriate surface quality and figure to achieve sub-arcminute performance has remained an elusive goal. In this paper, we report on new, thermally-formed glass micro-sheet optics capable of meeting the requirements of the next-generation of astronomical hard X-ray telescopes

Swift monitoring of Cygnus X-2: investigating the NUV-X-ray connection

The neutron star X-ray binary (NSXRB) Cygnus X-2 was observed by the Swift satellite 51 times over a 4 month period in 2008 with the XRT, UVOT, and BAT instruments. During this campaign, we observed Cyg X-2 in all three branches of the Z track (horizontal, normal, and flaring branches). We find that the NUV emission is uncorrelated with the soft X-ray flux detected with the XRT, and is anticorrelated with the BAT X-ray flux and the hard X-ray color. The observed anticorrelation is inconsistent with simple models of reprocessing as the source of the NUV emission. The anticorrelation may be a consequence of the high inclination angle of Cyg X-2, where NUV emission is preferentially scattered by a corona that expands as the disk is radiatively heated. Alternatively, if the accretion disk thickens as Cyg X-2 goes down the normal branch toward the flaring branch, this may be able to explain the observed anticorrelation. In these models the NUV emission may not be a good proxy for $\dot m$ in the system. We also discuss the implications of using Swift/XRT to perform spectral modeling of the continuum emission of NSXRBs.Comment: 10 pages, 8 figures. ApJ Accepte

Discovery of X-ray absorption features from the dipping low-mass X-ray binary XB 1916-053 with XMM-Newton

We report the discovery of narrow Fe XXV and Fe XXVI K alpha X-ray absorption lines at 6.65 and 6.95 keV in the persistent emission of the dipping low-mass X-ray binary (LMXB) XB 1916-053 during an XMM-Newton observation performed in September 2002. In addition, there is marginal evidence for absorption features at 1.48 keV, 2.67 kev, 7.82 keV and 8.29 keV consistent with Mg XII, S XVI, Ni XXVII K alpha and Fe XXVI K beta transitions, respectively. Such absorption lines from highly ionized ions are now observed in a number of high inclination (ie. close to edge-on) LMXBs, such as XB 1916-053, where the inclination is estimated to be between 60-80 degrees. This, together with the lack of any orbital phase dependence of the features (except during dips), suggests that the highly ionized plasma responsible for the absorption lines is located in a cylindrical geometry around the compact object. Using the ratio of Fe XXV and Fe XXVI column densities, we estimate the photo-ionization parameter of the absorbing material to be 10^{3.92} erg cm s^{-1}. Only the Fe XXV line is observed during dipping intervals and the upper-limits to the Fe XXVI column density are consistent with a decrease in the amount of ionization during dipping intervals. This implies the presence of cooler material in the line of sight during dipping. We also report the discovery of a 0.98 keV absorption edge in the persistent emission spectrum. The edge energy decreases to 0.87 keV during deep dipping intervals. The detected feature may result from edges of moderately ionized Ne and/or Fe with the average ionization level decreasing from persistent emission to deep dipping. This is again consistent with the presence of cooler material in the line of sight during dipping.Comment: 13 pages, accepted for publication in Astronomy and Astrophysic

Methylation status of Wnt signaling pathway genes affects the clinical outcome of Philadelphia-positive acute lymphoblastic leukemia

The clinical significance of aberrant promoter methylation of the canonical Wnt pathway antagonist genes (sFRP1, sFRP2, sFRP4, sFRP5, Wif1, Dkk3, and Hdpr1) and also putative tumor-suppressor gene Wnt5a, belonging to the non-canonical Wnt signaling pathway, was investigated in a large series of 75 patients with Philadelphia chromosome-positive acute lymphoblastic leukemia by methylationspecific polymerase chain reaction. At least one methylated gene was observed in cells from 66% (49/75) of patients (methylated group). Disease-free survival and overall survival at 9 years were 51 and 40%, respectively, for the unmethylated group and 3 and 2%, respectively, for the methylated group (both P < 0.0001). Multivariate analysis demonstrated that the Wnt methylation profile was an independent prognostic factor predicting disease-free survival (P = 0.007) and overall survival (P = 0.039). Abnormal DNA methylation of promoter-associated CpG islands in the Wnt signaling pathway is very common in Philadelphia chromosome-positive acute lymphoblastic leukemia and potentially defines subgroups with distinct clinical characteristics

MicroRNA expression profiling in Imatinib-resistant Chronic Myeloid Leukemia patients without clinically significant ABL1-mutations

The development of Imatinib Mesylate (IM), the first specific inhibitor of BCR-ABL1, has had a major impact in patients with Chronic Myeloid Leukemia (CML), establishing IM as the standard therapy for CML. Despite the clinical success obtained with the use of IM, primary resistance to IM and molecular evidence of persistent disease has been observed in 20-25% of IM treated patients. The existence of second generation TK inhibitors, which are effective in patients with IM resistance, makes identification of predictors of resistance to IM an important goal in CML. In this study, we have identified a group of 19 miRNAs that may predict clinical resistance to IM in patients with newly diagnosed CML

Epigenetic regulation of human cancer/testis antigen gene, HAGE, in chronic myeloid leukemia

Cancer testis antigens (CTA) provide attractive targets for cancer-specific immunotherapy. Although CTA genes are expressed in some normal tissues, such as the testis, this immunologically protected site lacks MHC I expression and as such, does not present self antigens to T cells. To date, CTA genes have been shown to be expressed in a range of solid tumors via demethylation of their promoter CpG islands, but rarely in chronic myeloid leukemia (CML) or other hematologic malignancies

BCR-ABL1-induced expression of HSPA8 promotes cell survival in chronic myeloid leukaemia

In order to determine new signal transduction pathways implicated in chronic myeloid leukaemia (CML), we performed a gene expression profile comparison between CD34+ cells from CML patients and healthy donors. Functional studies were performed using the Mo7e and Mo7e-p210 cell lines. Expression of CCND1 (Cyclin D1), as well as the chaperone HSPA8, which is important for regulation of CCND1, were significantly upregulated in CD34+ CML cells. Upregulation of HSPA8 was dependent, at least in part, on STAT5 (signal transducer and activator of transcrition 5)-dependent transcriptional activation, as demonstrated by chromatin immunoprecipitation. The presence of HSPA8 in the nuclear protein fraction as well as its binding to CCND1 suggests that it may contribute to stabilization of the CCND1/CDK4 complex, which, in turn, may participate in proliferation of CML cells. Treatment of CML cells with the specific HSPA8 inhibitor 15-deoxyspergualin induced inhibition of CML cell viability but did not induce apoptosis. In conclusion, our studies suggest that STAT5-mediated activation of HSPA8 induces nuclear translocation and activation of the CCND1/CDK4 complex leading to increased proliferation of CML cells, deciphering a new pathway implicated in CML and supporting a potential role of chaperone inhibitors in the treatment of CML