Detection of Pair-Superfluidity for bosonic mixtures in optical lattices

We consider a mixture of two bosonic species with tunable interspecies interaction in a periodic potential and discuss the advantages of low filling factors on the detection of the pair-superfluid phase. We show how the emergence of such a phase can be put dramatically into evidence by looking at the interference pictures and density correlations after expansion and by changing the interspecies interaction from attractive to repulsive.Comment: 4 pages, 4 figure

Bose-Einstein condensates in 1D optical lattices: compressibility, Bloch bands and elementary excitations

We discuss the Bloch-state solutions of the stationary Gross-Pitaevskii equation and of the Bogoliubov equations for a Bose-Einstein condensate in the presence of a one-dimensional optical lattice. The results for the compressibility, effective mass and velocity of sound are analysed as a function of the lattice depth and of the strength of the two-body interaction. The band structure of the spectrum of elementary excitations is compared with the one exhibited by the stationary solutions (``Bloch bands''). Moreover, the numerical calculations are compared with the analytic predictions of the tight binding approximation. We also discuss the role of quantum fluctuations and show that the condensate exhibits 3D, 2D or 1D features depending on the lattice depth and on the number of particles occupying each potential well. We finally show how, using a local density approximation, our results can be applied to study the behaviour of the gas in the presence of harmonic trapping.Comment: version published in EPJ

Topological two-body bound states in the interacting Haldane model

We study the topological properties of the two-body bound states in an interacting Haldane model as a function of interparticle interactions. In particular, we identify topological phases where the two-body edge states have either the same or the opposite chirality as compared to single-particle edge states. We highlight that in the moderately interacting regime, which is relevant for the experimental realization with ultracold atoms, the topological transition is affected by the internal structure of the bound state, and the phase boundaries are consequently deformed

Beyond the Landau Criterion for Superfluidity

According to the Landau criterion for superfluidity, a Bose-Einstein condensate flowing with a group velocity smaller than the sound velocity is energetically stable to the presence of perturbing potentials. We found that this is strictly correct only for vanishingly small perturbations. The superfluid critical velocity strongly depends on the strength and shape of the defect. We quantitatively study, both numerically and with an approximate analytical model, the dynamical response of a one-dimensional condensate flowing against an istantaneously raised spatially periodic defect. We found that the critical velocity $v_c$ decreases by incresing the strength of the defect $V_0$, up to to a critical value of the defect intensity where the critical velocity vanishes

Quantum fluctuations beyond the Gutzwiller approximation in the Bose-Hubbard model

We develop a quantum many-body theory of the Bose-Hubbard model based on the canonical quantization of the action derived from a Gutzwiller mean-field ansatz. Our theory is a systematic generalization of the Bogoliubov theory of weakly interacting gases. The control parameter of the theory, defined as the zero point fluctuations on top of the Gutzwiller mean-field state, remains small in all regimes. The approach provides accurate results throughout the whole phase diagram, from the weakly to the strongly interacting superfluid and into the Mott insulating phase. As specific examples of application, we study the two-point correlation functions, the superfluid stiffness, and the density fluctuations, for which quantitative agreement with available quantum Monte Carlo data is found. In particular, the two different universality classes of the superfluid-insulator quantum phase transition at integer and noninteger filling are recovered

Light scattering by ultracold atoms in an optical lattice

We investigate theoretically light scattering of photons by ultracold atoms in an optical lattice in the linear regime. A full quantum theory for the atom-photon interactions is developed as a function of the atomic state in the lattice along the Mott-insulator -- superfluid phase transition, and the photonic scattering cross section is evaluated as a function of the energy and of the direction of emission. The predictions of this theory are compared with the theoretical results of a recent work on Bragg scattering in time-of-flight measurements [A.M. Rey, {\it et al.}, Phys. Rev. A {\bf 72}, 023407 (2005)]. We show that, when performing Bragg spectroscopy with light scattering, the photon recoil gives rise to an additional atomic site to site hopping, which can interfere with ordinary tunneling of matter waves and can significantly affect the photonic scattering cross section.Comment: 13 pages, 6 fig, (accepted in PRA

Regulation of CD45 phosphatase by oncogenic ALK in anaplastic large cell lymphoma

Anaplastic Large Cell Lymphoma (ALCL) is a subtype of non-Hodgkin lymphoma frequently driven by the chimeric tyrosine kinase NPM-ALK, generated by the t (2,5)(p23;q35) translocation. While ALK+ ALCL belongs to mature T cell lymphomas, loss of T cell identity is observed in the majority of ALCL secondary to a transcriptional and epigenetic repressive program induced by oncogenic NPM-ALK. While inhibiting the expression of T cell molecules, NPM-ALK activates surrogate TCR signaling by directly inducing pathways downstream the TCR. CD45 is a tyrosine phosphatase that plays a central role in T cell activation by controlling the TCR signaling and regulating the cytokine responses through the JAK/STAT pathway and exists in different isoforms depending on the stage of T-cell maturation, activation and differentiation. ALK+ ALCL cells mainly express the isoform CD45RO in keeping with their mature/memory T cell phenotype. Because of its regulatory effect on the JAK/STAT pathway that is essential for ALK+ ALCL, we investigated whether CD45 expression was affected by oncogenic ALK. We found that most ALK+ ALCL cell lines express the CD45RO isoform with modest CD45RA expression and that NPM-ALK regulated the expression of these CD45 isoforms. Regulation of CD45 expression was dependent on ALK kinase activity as CD45RO expression was increased when NPM-ALK kinase activity was inhibited by treatment with ALK tyrosine kinase inhibitors (TKIs). Silencing ALK expression through shRNA or degradation of ALK by the PROTAC TL13-112 caused upregulation of CD45RO both at mRNA and protein levels with minimal changes on CD45RA, overall indicating that oncogenic ALK downregulates the expression of CD45. CD45 repression was mediated by STAT3 as demonstrated by ChIP-seq data on ALCL cells treated with the ALK-TKI crizotinib or cells treated with a STAT3 degrader. Next, we found that knocking-out CD45 with the CRISPR/Cas9 system resulted in increased resistance to ALK TKI treatment and CD45 was down-regulated in ALCL cells that developed resistance in vitro to ALK TKIs. Overall, these data suggest that CD45 expression is regulated by ALK via STAT3 and acts as a rheostat of ALK oncogenic signaling and resistance to TKI treatment in ALCL

Collective oscillations of a 1D trapped Bose gas

Starting from the hydrodynamic equations of superfluids, we calculate the frequencies of the collective oscillations of a harmonically trapped Bose gas for various 1D configurations. These include the mean field regime described by Gross-Pitaevskii theory and the beyond mean field regime at small densities described by Lieb-Liniger theory. The relevant combinations of the physical parameters governing the transition between the different regimes are discussed.Comment: 4 pages, 2 figure

Excess of NPM-ALK oncogenic signaling promotes cellular apoptosis and drug dependency.

Most of the anaplastic large-cell lymphoma (ALCL) cases carry the t(2;5; p23;q35) that produces the fusion protein NPM-ALK (nucleophosmin-anaplastic lymphoma kinase). NPM-ALK-deregulated kinase activity drives several pathways that support malignant transformation of lymphoma cells. We found that in ALK-rearranged ALCL cell lines, NPM-ALK was distributed in equal amounts between the cytoplasm and the nucleus. Only the cytoplasmic portion was catalytically active in both cell lines and primary ALCL, whereas the nuclear portion was inactive because of heterodimerization with NPM1. Thus, about 50% of the NPM-ALK is not active and sequestered as NPM-ALK/NPM1 heterodimers in the nucleus. Overexpression or relocalization of NPM-ALK to the cytoplasm by NPM genetic knockout or knockdown caused ERK1/2 (extracellular signal-regulated protein kinases 1 and 2) increased phosphorylation and cell death through the engagement of an ATM/Chk2- and γH2AX (phosphorylated H2A histone family member X)-mediated DNA-damage response. Remarkably, human NPM-ALK-amplified cell lines resistant to ALK tyrosine kinase inhibitors (TKIs) underwent apoptosis upon drug withdrawal as a consequence of ERK1/2 hyperactivation. Altogether, these findings indicate that an excess of NPM-ALK activation and signaling induces apoptosis via oncogenic stress responses. A 'drug holiday' where the ALK TKI treatment is suspended could represent a therapeutic option in cells that become resistant by NPM-ALK amplification.We thank Maria Stella Scalzo for technical support, Dr Emanuela Colombo for kindly providing MEFs that lack NPM1 (MEF NPM−/−p53−/−) and control fibroblasts (MEF p53−/−), Dr Guido Serini for the use of his confocal microscopy unit at the Candiolo Cancer Institute—IRCCS, Torino, Italy. We also thank Ariad Pharmaceutical, Pfizer, Astellas and Novartis that kindly provided all drugs used in this study. This work was supported by the Regione Lombardia (ID14546A) and Fondazione Berlucchi Onlus Grant 2014 (to CGP), and by grants FP7 ERC-2009-StG (Proposal No. 242965—‘Lunely’); Associazione Italiana per la Ricerca sul Cancro (AIRC) Grant IG-12023; Koch Institute/DFCC Bridge Project Fund; Ellison Foundation Boston; Worldwide Cancer Research Association (former AICR) grant 12-0216; the Grant for Oncology Innovation by Merck-Serono and R01 CA196703-01 (to RC).This is the author accepted manuscript. The final version is available from NPG via http://dx.doi.org/10.1038/onc.2015.45