Impurity effect on weak anti-localization in the topological insulator Bi2Te3

We study weak anti-localization (WAL) effect in topological insulator Bi2Te3 thin films at low temperatures. Two-dimensional WAL effect associated with surface carriers is revealed in the tilted magnetic field dependence of magneto-conductance. Our data demonstrates that the observed WAL is robust against deposition of non-magnetic Au impurities on the surface of the thin films. But it is quenched by deposition of magnetic Fe impurities which destroy the pi Berry's phase of the topological surface states. The magneto-conductance data of a 5 nm Bi2Te3 film suggests that a crossover from symplectic to unitary classes is observed with the deposition of Fe impurities.Comment: 4 pages, 3 figures. Corresponding author email address: [email protected]

Medium effect on photon production in ultrarelativistic nuclear collisions

The effect of in-medium vector and axial-vector meson masses on photon production is studied. We assume that the effective mass of a vector meson in hot nuclear matter decreases according to a universal scaling law, while that of an axial-vector meson is given by Weinberg's mass formula. We find that the thermal production rate of photons increases with reduced masses, and is enhanced by an order of magnitude at T=160 MeV with $m_\rho=300$ MeV. Assuming a hydrodynamic evolution, we estimate the effect of the reduced masses on photon production in nucleus-nucleus collisions. The result is compared to experimental data from the WA80/WA98 collaboration.Comment: 21 pages, REVTEX + 9 figures (ps file

TWEAK-FN14 signaling induces lysosomal degradation of a cIAP1–TRAF2 complex to sensitize tumor cells to TNFα

Synthetic inhibitor of apoptosis (IAP) antagonists induce degradation of IAP proteins such as cellular IAP1 (cIAP1), activate nuclear factor κB (NF-κB) signaling, and sensitize cells to tumor necrosis factor α (TNFα). The physiological relevance of these discoveries to cIAP1 function remains undetermined. We show that upon ligand binding, the TNF superfamily receptor FN14 recruits a cIAP1–Tnf receptor-associated factor 2 (TRAF2) complex. Unlike IAP antagonists that cause rapid proteasomal degradation of cIAP1, signaling by FN14 promotes the lysosomal degradation of cIAP1–TRAF2 in a cIAP1-dependent manner. TNF-like weak inducer of apoptosis (TWEAK)/FN14 signaling nevertheless promotes the same noncanonical NF-κB signaling elicited by IAP antagonists and, in sensitive cells, the same autocrine TNFα-induced death occurs. TWEAK-induced loss of the cIAP1–TRAF2 complex sensitizes immortalized and minimally passaged tumor cells to TNFα-induced death, whereas primary cells remain resistant. Conversely, cIAP1–TRAF2 complex overexpression limits FN14 signaling and protects tumor cells from TWEAK-induced TNFα sensitization. Lysosomal degradation of cIAP1–TRAF2 by TWEAK/FN14 therefore critically alters the balance of life/death signals emanating from TNF-R1 in immortalized cells

Notch ligation by Delta1 inhibits peripheral immune responses to transplantation antigens by a CD8⁺ cell–dependent mechanism

Notch signaling plays a fundamental role in determining the outcome of differentiation processes in many tissues. Notch signaling has been implicated in T versus B cell lineage commitment, thymic differentiation, and bone marrow hematopoietic precursor renewal and differentiation. Notch receptors and their ligands are also expressed on the surface of mature lymphocytes and APCs, but the effects of Notch signaling in the peripheral immune system remain poorly defined. The aim of the studies reported here was to investigate the effects of signaling through the Notch receptor using a ligand of the Delta-like family. We show that Notch ligation in the mature immune system markedly decreases responses to transplantation antigens. Constitutive expression of Delta-like 1 on alloantigen-bearing cells renders them nonimmunogenic and able to induce specific unresponsiveness to a challenge with the same alloantigen, even in the form of a cardiac allograft. These effects could be reversed by depletion of CD8⁺ cells at the time of transplantation. Ligation of Notch on splenic CD8⁺ cells results in a dramatic decrease in IFN-γ with a concomitant enhancement of IL-10 production, suggesting that Notch signaling can alter the differentiation potential of CD8⁺ cells. These data implicate Notch signaling in regulation of peripheral immunity and suggest a novel approach for manipulating deleterious immune responses

Accuracy and cost-effectiveness of dynamic contrast-enhanced CT in the characterisation of solitary pulmonary nodules — the SPUtNIk study

$\textbf{Introduction:}$ Solitary pulmonary nodules (SPNs) are common on CT. The most cost-effective investigation algorithm is still to be determined. Dynamic contrastenhanced CT (DCE-CT) is an established diagnostic test not widely available in the UK currently. $\textbf{Methods and analysis:}$ The SPUtNIk study will assess the diagnostic accuracy, clinical utility and cost-effectiveness of DCE-CT, alongside the current CT and 18-flurodeoxyglucose-positron emission tomography) ($^{18}$FDG-PET)-CT nodule characterisation strategies in the National Health Service (NHS). Image acquisition and data analysis for $^{18}$FDG-PET-CT and DCE-CT will follow a standardised protocol with central review of 10% to ensure quality assurance. Decision analytic modelling will assess the likely costs and health outcomes resulting from incorporation of DCE-CT into management strategies for patients with SPNs. $\textbf{Ethics and dissemination:}$ Approval has been granted by the South West Research Ethics Committee. Ethics reference number 12/SW/0206. The results of the trial will be presented at national and international meetings and published in an Health Technology Assessment (HTA) Monograph and in peer-reviewed journals.The trial is funded by the National Institute for Health Research HTA Programme (grant no: 09/22/117) and is being run by Southampton Clinical Trials Unit, directed by Professor Gareth Griffiths and part funded by Cancer Research UK. NRQ and RCR are part funded by the Cambridge Biomedical Research Centre and the Cancer Research Network: Eastern