Search for right-handed W bosons in top quark decay

We present a measurement of the fraction f+ of right-handed W bosons produced in top quark decays, based on a candidate sample of $t\bar{t}$ events in the lepton+jets decay mode. These data correspond to an integrated luminosity of 230pb^-1, collected by the DO detector at the Fermilab Tevatron $p\bar{p}$ Collider at sqrt(s)=1.96 TeV. We use a constrained fit to reconstruct the kinematics of the $t\bar{t}$ and decay products, which allows for the measurement of the leptonic decay angle $\theta^*$ for each event. By comparing the $\cos\theta^*$ distribution from the data with those for the expected background and signal for various values of f+, we find f+=0.00+-0.13(stat)+-0.07(syst). This measurement is consistent with the standard model prediction of f+=3.6x10^-4.Comment: Submitted to Physical Review D Rapid Communications 7 pages, 3 figure

Met-Independent Hepatocyte Growth Factor-mediated regulation of cell adhesion in human prostate cancer cells

BACKGROUND: Prostate cancer cells communicate reciprocally with the stromal cells surrounding them, inside the prostate, and after metastasis, within the bone. Each tissue secretes factors for interpretation by the other. One stromally-derived factor, Hepatocyte Growth Factor (HGF), was found twenty years ago to regulate invasion and growth of carcinoma cells. Working with the LNCaP prostate cancer progression model, we found that these cells could respond to HGF stimulation, even in the absence of Met, the only known HGF receptor. The new HGF binding partner we find on the cell surface may help to clarify conflicts in the past literature about Met expression and HGF response in cancer cells. METHODS: We searched for Met or any HGF binding partner on the cells of the PC3 and LNCaP prostate cancer cell models, using HGF immobilized on agarose beads. By using mass spectrometry analyses and sequencing we have identified nucleolin protein as a novel HGF binding partner. Antibodies against nucleolin (or HGF) were able to ameliorate the stimulatory effects of HGF on met-negative prostate cancer cells. Western blots, RT-PCR, and immunohistochemistry were used to assess nucleolin levels during prostate cancer progression in both LNCaP and PC3 models. RESULTS: We have identified HGF as a major signaling component of prostate stromal-conditioned media (SCM) and have implicated the protein nucleolin in HGF signal reception by the LNCaP model prostate cancer cells. Antibodies that silence either HGF (in SCM) or nucleolin (on the cell surfaces) eliminate the adhesion-stimulatory effects of the SCM. Likewise, addition of purified HGF to control media mimics the action of SCM. C4-2, an LNCaP lineage-derived, androgen-independent human prostate cancer cell line, responds to HGF in a concentration-dependent manner by increasing its adhesion and reducing its migration on laminin substratum. These HGF effects are not due to shifts in the expression levels of laminin-binding integrins, nor can they be linked to expression of the known HGF receptor Met, as neither LNCaP nor clonally-derived C4-2 sub-line contain any detectable Met protein. Even in the absence of Met, small GTPases are activated, linking HGF stimulation to membrane protrusion and integrin activation. Membrane-localized nucelolin levels increase during cancer progression, as modeled by both the PC3 and LNCaP prostate cancer progression cell lines. CONCLUSION: We propose that cell surface localized nucleolin protein may function in these cells as a novel HGF receptor. Membrane localized nucleolin binds heparin-bound growth factors (including HGF) and appears upregulated during prostate cancer progression. Antibodies against nucleolin are able to ameliorate the stimulatory effects of HGF on met-negative prostate cancer cells. HGF-nucleolin interactions could be partially responsible for the complexity of HGF responses and met expression reported in the literature

Loss Modeling for Interlocked Magnetic Cores

In mass production, interlocks are an affordable staking solution for magnetic cores of electrical machines. However, the interlock dowels introduce an increase of core losses, not only for the appearance of conductive paths in the interlock regions, but also for a non-negligible worsening of the magnetic material properties (including the hysteresis losses), both inside the interlocks and in the surrounding areas. This study aims at developing a reliable and accurate three-dimensional FEM model that takes into account the contact resistance between interlocks and laminations, as well as layered regions constituted by damaged materials. The paper includes modelling hints and the fine-tuning of the 3D FEM that includes a detailed modeling of the interlock section. Examples of flux and eddy current density distributions are provided, together with the computation of the total iron losses for a variable number of rectangular dowels in the yoke of stator core samples. The numerical results are validated by experimental measurements conducted on multiple samples having different number of interlocks

Experimental Assessment and Modeling of Losses in Interlocked Magnetic Cores

The use of interlocks often represents an affordable stacking solution for soft magnetic cores in mass production of electrical machines. However, due to the process itself, the material behavior and thus the resulting electrical machine performance is negatively impacted. On the one hand, this is due to additional conductive paths, which increase the eddy current losses. On the other hand, locally introduced mechanical stresses occur. These lead to nonnegligible degradation of the magnetic material properties inside and around the interlock area, following higher hysteresis losses. This article investigates and develops a reliable and accurate three-dimensional finite-element method model that considers the contact resistance between interlocks and laminations, as well as layered regions for the material degradation around the interlock area. Examples of flux and eddy current density distributions are provided, together with the computation of the total iron losses for a variable number of rectangular dowels in the yoke of stator core samples. The numerical analyses are validated by several interlaboratory measurements conducted on multiple stator core samples made of two different grades of electrical steels and with different numbers of interlocks. Results reveal impact of some percent on the core losses and well evident degradation on the material BH curve

Spatial MMF Harmonic Mitigation in Aluminum-Cage Induction Motors

This study investigates the effects of the spatial harmonics of magneto-motive force that appear in the air-gap of aluminum-cage induction motors, proposing some techniques for their mitigation. With respect to previous researches, special magnetic wedges to be mounted in the stator opening regions of semi-closed slots of existing motors are proposed, together with a special winding layout having a very low magnetomotive force harmonic content. Both 2D- and 3D-FEM numerical simulations have been carried out to quantify the problems and to understand the potential benefits of inserting the stator wedges. At the end, the mechanical feasibility of the proposed wedges is considered together with some attempts at implementation

Activation of Stimulator of Interferon Genes (STING) and Sjogren Syndrome

Sjogren syndrome (SS), a chronic autoimmune disorder causing dry mouth, adversely affects the overall oral health in patients. Activation of innate immune responses and excessive production of type I interferons (IFNs) play a critical role in the pathogenesis of this disorder. Recognition of nucleic acids by cytosolic nucleic acid sensors is a major trigger for the induction of type I IFNs. Upon activation, cytosolic DNA sensors can interact with the stimulator of interferon genes (STING) protein, and activation of STING causes increased expression of type I IFNs. The role of STING activation in SS is not known. In this study, to investigate whether the cytosolic DNA sensing pathway influences SS development, female C57BL/6 mice were injected with a STING agonist, dimethylxanthenone-4-acetic acid (DMXAA). Salivary glands (SGs) were studied for gene expression and inflammatory cell infiltration. SG function was evaluated by measuring pilocarpine-induced salivation. Sera were analyzed for cytokines and autoantibodies. Primary SG cells were used to study the expression and activation of STING. Our data show that systemic DMXAA treatment rapidly induced the expression of Ifnb1, Il6, and Tnfa in the SGs, and these cytokines were also elevated in circulation. In contrast, increased Ifng gene expression was dominantly detected in the SGs. The type I innate lymphoid cells present within the SGs were the major source of IFN-gamma, and their numbers increased significantly within 3 d of treatment. STING expression in SGs was mainly observed in ductal and interstitial cells. In primary SG cells, DMXAA activated STING and induced IFN-beta production. The DMXAA-treated mice developed autoantibodies, sialoadenitis, and glandular hypofunction. Our study demonstrates that activation of the STING pathway holds the potential to initiate SS. Thus, apart from viral infections, conditions that cause cellular perturbations and accumulation of host DNA within the cytosol should also be considered as possible triggers for SS