Ramsey interferometry with an atom laser

We present results on a free-space atom interferometer operating on the first order magnetically insensitive |F=1,mF=0> -> |F=2,mF=0> transition of Bose-condensed 87Rb atoms. A pulsed atom laser is output-coupled from a Bose-Einstein condensate and propagates through a sequence of two internal state beam splitters, realized via coherent Raman transitions between the two interfering states. We observe Ramsey fringes with a visibility close to 100% and determine the current and the potentially achievable interferometric phase sensitivity. This system is well suited to testing recent proposals for generating and detecting squeezed atomic states.Comment: published version, 8 pages, 3 figure

Theoretical Analysis of a Large Momentum Beamsplitter using Bloch Oscillations

In this paper, we present the implementation of Bloch oscillations in an atomic interferometer to increase the separation of the two interfering paths. A numerical model, in very good agreement with the experiment, is developed. The contrast of the interferometer and its sensitivity to phase fluctuations and to intensity fluctuations are also calculated. We demonstrate that the sensitivity to phase fluctuations can be significantly reduced by using a suitable arrangement of Bloch oscillations pulses

CpG Islands: Starting Blocks for Replication and Transcription

International audienc

Testing new physics with the electron g-2

We argue that the anomalous magnetic moment of the electron (a_e) can be used to probe new physics. We show that the present bound on new-physics contributions to a_e is 8*10^-13, but the sensitivity can be improved by about an order of magnitude with new measurements of a_e and more refined determinations of alpha in atomic-physics experiments. Tests on new-physics effects in a_e can play a crucial role in the interpretation of the observed discrepancy in the anomalous magnetic moment of the muon (a_mu). In a large class of models, new contributions to magnetic moments scale with the square of lepton masses and thus the anomaly in a_mu suggests a new-physics effect in a_e of (0.7 +- 0.2)*10^-13. We also present examples of new-physics theories in which this scaling is violated and larger effects in a_e are expected. In such models the value of a_e is correlated with specific predictions for processes with violation of lepton number or lepton universality, and with the electric dipole moment of the electron.Comment: 34 pages, 7 figures. Minor changes and references adde

SUSY_FLAVOR v2.5: a computational tool for FCNC and CP-violating processes in the MSSM

We present SUSY_FLAVOR version 2.5 - a Fortran 77 program that calculates low-energy flavor observables in the general $R$-parity conserving MSSM. For a set of MSSM parameters as input, the code gives predictions for: 1. Electric dipole moments of the leptons and the neutron. 2. Anomalous magnetic moments (i.e. $g-2$) of the leptons. 3. Radiative lepton decays ($\mu\to e\gamma$ and $\tau\to \mu\gamma, e\gamma$). 4. Rare Kaon decays ($K^0_L\to \pi^0\bar\nu\nu$ and $K^+\to \pi^+ \bar\nu\nu$). 5. Leptonic $B$ decays ($B_{s,d}\to l^+ l^-$, $B\to \tau \nu$, $B\to D \tau \nu$ and $B\to D^\star \tau \nu$). 6. Radiative $B$ decays ($B\to\bar X_s \gamma$). 7. Rare decays of top quark to Higgs boson ($t\to ch,uh$). 8. $\Delta F=2$ processes ($\bar K^0-K^0$, $\bar D-D$, $\bar B_d-B_d$ and $\bar B_s-B_s$ mixing). SUSY_FLAVOR performs the resummation of all chirally enhanced corrections, i.e. takes into account the effects enhanced by $\tan\beta$ and/or large trilinear soft mixing terms to all orders in perturbation theory. All calculations are done using exact diagonalization of the sfermion mass matrices. Comparing to previous versions, in SUSY_FLAVOR v2.5 parameter initialization in SLHA2 format has been significantly generalized and simplified, so that program accepts without modifications most of the output files produced by other codes calculating MSSM spectra and processes. In addition, the routine calculating branching ratios for rare decays of top quark to Higgs boson has been included. The program can be obtained from www.fuw.edu.pl/susy_flavor.Comment: Updated from arXiv:1003.4260 [hep-ph] (SUSY_FLAVOR v1 manual), 61 pages; updated sections on modified user interface and on newly added processes. SUSY_FLAVOR code available at http://www.fuw.edu.pl/susy_flavo

Charged-Lepton Flavour Physics

This writeup of a talk at the 2011 Lepton-Photon symposium in Mumbai, India, summarises recent results in the charged-lepton flavour sector. I review searches for charged-lepton flavour violation, lepton electric dipole moments and flavour-conserving CP violation. I also discuss recent progress in tau-lepton physics and in the Standard Model prediction of the muon anomalous magnetic moment.Comment: Presented at Lepton-Photon 2011, Mumbai, India; 23 pages, 14 figure

Risk of Myocardial Infarction in Parents of HIV-infected Individuals: a population-based Cohort Study

<p>Abstract</p> <p>Background</p> <p>Previous studies have indicated an increased risk of myocardial infarction (MI) in HIV infected individuals especially after start of highly active antiretroviral therapy (HAART). It is however controversial whether the increased risk of atherosclerotic disease is exclusively associated with the HIV disease and HAART or whether life-style related or genetic factors also increase the risk in this population. To establish whether the increased risk of myocardial infarction in HIV patients partly reflects an increased risk of MI in their families, we estimated the relative risk of MI in parents of HIV-infected individuals.</p> <p>Methods</p> <p>From the Danish HIV Cohort Study and the Danish Civil Registration System we identified the parents of all HIV-infected patients born in Denmark after 1952 in whom a Danish born mother was identifiable. For each HIV patient, 4 matched population controls and their parents were identified. Cumulative incidence functions were constructed to illustrate time to first MI of the parents as registered in the Danish National Hospital Registry. Incidence rate ratios (IRR) were estimated by Cox's regression analyses. Due to the confidential type of the analysed data the study was approved by the Danish Data Protection Agency.</p> <p>Results</p> <p>2,269 mothers and 2,022 fathers of HIV patients as well as 9,076 mothers and 8,460 fathers of control subjects were identified. We observed an increased risk of MI in mothers of HIV patients (adjusted IRR, 1.31; 95% CI: 1.08-1.60). The strongest association was seen in case the offspring was infected heterosexually (adjusted IRR, 1.59; 95% CI: 1.07-2.35) or by IV drug abuse (IVD) (adjusted IRR, 1.63; 95% CI: 1.02-2.60). In fathers of HIV patients the risk of MI was only increased if the offspring was infected by IVD (adjusted IRR, 1.42; 95% CI: 1.01-2.00).</p> <p>Conclusion</p> <p>Mothers of HIV-infected patients have an increased risk of MI. We presume that this stems from family related life style risk factors, some of which may also influence the risk of MI in HIV-infected patients.</p

Glutamine depletion by crisantaspase hinders the growth of human hepatocellular carcinoma xenografts

Background: A subset of human hepatocellular carcinomas (HCC) exhibit mutations of β-catenin gene CTNNB1 and overexpress Glutamine synthetase (GS). The CTNNB1-mutated HCC cell line HepG2 is sensitive to glutamine starvation induced in vitro with the antileukemic drug Crisantaspase and the GS inhibitor methionine-L-sulfoximine (MSO). Methods: Immunodeficient mice with subcutaneous xenografts of the CTNNB1-mutated HCC cell lines HepG2 and HC-AFW1 were treated with Crisantaspase and/or MSO, and tumour growth was monitored. At the end of treatment, tumour weight and histology were assessed. Serum and tissue amino acids were determined by HPLC. Gene and protein expression were estimated with RT-PCR and western blot and GS activity with a colorimetric method. mTOR activity was evaluated from the phosphorylation of p70S6K1. Results: Crisantaspase and MSO depleted serum glutamine, lowered glutamine in liver and tumour tissue, and inhibited liver GS activity. HepG2 tumour growth was significantly reduced by either Crisantaspase or MSO, and completely suppressed by the combined treatment. The combined treatment was also effective against xenografts of the HC-AFW1 cell line, which is Crisantaspase resistant in vitro. Conclusions: The combination of Crisantaspase and MSO reduces glutamine supply to CTNNB1-mutated HCC xenografts and hinders their growth

β-Catenin Loss in Hepatocytes Promotes Hepatocellular Cancer after Diethylnitrosamine and Phenobarbital Administration to Mice

Hepatocellular Carcinoma (HCC) is the fifth most common cancer worldwide. β-Catenin, the central orchestrator of the canonical Wnt pathway and a known oncogene is paramount in HCC pathogenesis. Administration of phenobarbital (PB) containing water (0.05% w/v) as tumor promoter following initial injected intraperitoneal (IP) diethylnitrosamine (DEN) injection (5 µg/gm body weight) as a tumor inducer is commonly used model to study HCC in mice. Herein, nine fifteen-day male β-catenin knockout mice (KO) and fifteen wild-type littermate controls (WT) underwent DEN/PB treatment and were examined for hepatic tumorigenesis at eight months. Paradoxically, a significantly higher tumor burden was observed in KO (p<0.05). Tumors in KO were β-catenin and glutamine synthetase negative and HGF/Met, EGFR & IGFR signaling was unremarkable. A significant increase in PDGFRα and its ligand PDGF-CC leading to increased phosphotyrosine-720-PDGFRα was observed in tumor-bearing KO mice (p<0.05). Simultaneously, these livers displayed increased cell death, stellate cell activation, hepatic fibrosis and cell proliferation. Further, PDGF-CC significantly induced hepatoma cell proliferation especially following β-catenin suppression. Our studies also demonstrate that the utilized DEN/PB protocol in the WT C57BL/6 mice did not select for β-catenin gene mutations during hepatocarcinogenesis. Thus, DEN/PB enhanced HCC in mice lacking β-catenin in the liver may be due to their ineptness at regulating cell survival, leading to enhanced fibrosis and regeneration through PDGFRα activation. β-Catenin downregulation also made hepatoma cells more sensitive to receptor tyrosine kinases and thus may be exploited for therapeutics