In this letter we present an experimental study of the collective dipole oscillation of a spin-orbit coupled Bose-Einstein condensate in a harmonic trap. Dynamics of the center-of-mass dipole oscillation is studied in a broad parameter region, as a function of spin-orbit coupling parameters as well as oscillation amplitude. Anharmonic properties beyond effective-mass approximation are revealed, such as amplitude-dependent frequency and finite oscillation frequency at place with divergent effective mass. These anharmonic behaviors agree quantitatively with variational wave-function calculations. Moreover, we experimentally demonstrate a unique feature of spin-orbit coupled system predicted by a sum-rule approach, stating that spin polarization susceptibility-a static physical quantity-can be measured via dynamics of dipole oscillation. The divergence of polarization susceptibility is observed at the quantum phase transition that separates magnetic nonzero-momentum condensate from nonmagnetic zero-momentum phase. The good agreement between the experimental and theoretical results provides a bench mark for recently developed theoretical approaches.Many interesting quantum phases can emerge in solid state materials when electrons are placed in a strong magnetic field or possess strong spin-orbit (SO) coupling, such as the fractional quantum Hall effect [1] and the topological insulator [2]. In cold atom systems, albeit neutral atoms have neither charges nor SO coupling, the recent exciting experimental progress demonstrates that artificial gauge potentials can be synthesized in laboratory by laser control technique [3][4][5][6][7][8][9][10]. Synthetic gauge potential is becoming a powerful tool for simulating real materials with cold atoms. Moreover, the system of SO coupled bosons does not have an analogy in conventional condensed matter systems, and can exhibit many novel phases [11] such as striped superfluid phase [12,13] and half vortex phase [14][15][16][17].Collective excitations play an important role in studying physical properties of trapped atomic Bose-Einstein condensates (BEC) and degenerate Fermi gases. Collective dipole oscillation is a center-of-mass motion of all atoms. For a conventional condensate, the dipole oscillation is trivial: the frequency is just the harmonictrap frequency, independent of oscillation amplitude and interatomic interaction. This is known as Kohn theorem [18,19]. For a SO coupled condensate, however, it was found [4] that the dipole-oscillation frequency deviates from the trap frequency and the experimental data thereby can be explained by effective-mass approximation. Recently, much theoretical effort has been taken to understand dynamics of a SO coupled BEC [20][21][22][23][24][25], and many predicted unconventional properties remain to be experimentally explored. In particular, the so-called sum-rule approach predicts [25] a unique feature of SO coupled condensate: spin polarization susceptibility-a static physical quantity-can be measured via dynamics of dipole oscillatio...

The Wiskott-Aldrich syndrome protein (WASp) has been implicated in modulation of lymphocyte activation and cytoskeletal reorganization. To address the mechanisms whereby WASp subserves such functions, we have examined WASp roles in lymphocyte development and activation using mice carrying a WAS null allele (WAS − / −). Enumeration of hemopoietic cells in these animals revealed total numbers of thymocytes, peripheral B and T lymphocytes, and platelets to be significantly diminished relative to wild-type mice. In the thymus, this abnormality was associated with impaired progression from the CD44−CD25+ to the CD44−CD25− stage of differentiation. WASp-deficient thymocytes and T cells also exhibited impaired proliferation and interleukin (IL)-2 production in response to T cell antigen receptor (TCR) stimulation, but proliferated normally in response to phorbol ester/ionomycin. This defect in TCR signaling was associated with a reduction in TCR-evoked upregulation of the early activation marker CD69 and in TCR-triggered apoptosis. While induction of TCR-ζ, ZAP70, and total protein tyrosine phosphorylation as well as mitogen-activated protein kinase (MAPK) and stress-activated protein/c-Jun NH2-terminal kinase (SAPK/JNK) activation appeared normal in TCR-stimulated WAS − / − cells, TCR-evoked increases in intracellular calcium concentration were decreased in WASp-deficient relative to wild-type cells. WAS − / − lymphocytes also manifested a marked reduction in actin polymerization and both antigen receptor capping and endocytosis after TCR stimulation, whereas WAS − / − neutrophils exhibited reduced phagocytic activity. Together, these results provide evidence of roles for WASp in driving lymphocyte development, as well as in the translation of antigen receptor stimulation to proliferative or apoptotic responses, cytokine production, and cytoskeletal rearrangement. The data also reveal a role for WASp in modulating endocytosis and phagocytosis and, accordingly, suggest that the immune deficit conferred by WASp deficiency reflects the disruption of a broad range of cellular behaviors.

A variant of the PTPN22-encoded Lyp phosphatase (Lyp620W) confers risk for autoimmune disease, but the mechanisms underlying this association remain unclear. We show here that mice expressing the Lyp variant homolog Pep619W manifest thymic and splenic enlargement accompanied by increases in T-cell number, activation and positive selection and in dendritic- and B-cell activation. Although Ptpn22 (Pep) transcript levels were comparable in Pep619W and wild-type Pep619R mice, Pep protein levels were dramatically reduced in the mutant mice, with Pep619W protein being more rapidly degraded and showing greater association with and in vitro cleavage by calpain 1 than Pep619R. Similarly, levels of the Lyp620W variant were decreased in human T and B cells, and its calpain binding and cleavage were increased relative to wild-type Lyp620R. Thus, calpain-mediated degradation with consequently reduced Lyp/Pep expression and lymphocyte and dendritic cell hyperresponsiveness represents a mechanism whereby Lyp620W may increase risk for autoimmune disease.