Preparation of one 87Rb and one 133Cs atom in a single optical tweezer

We report the preparation of exactly one 87Rb atom and one133Cs atom in the same optical tweezer as the essential first step towards the construction of a tweezer array of individually trapped 87Rb133Cs molecules. Through careful selection of the tweezer wavelengths, we show how to engineer species-selective trapping potentials suitable for high-fidelity preparation of Rb + Cs atom pairs. Using a wavelength of 814 nm to trap Rb and 938 nm to trap Cs, we achieve loading probabilities of 0.508(6) for Rb and 0.547(6) for Cs using standard red-detuned molasses cooling. Loading the traps sequentially yields exactly one Rb and one Cs atom in 28.4(6) % of experimental runs. Using a combination of an acousto-optic deflector and a piezo-controlled mirror to control the relative position of the tweezers, we merge the two tweezers, retaining the atom pair with a probability of 0.99(+0.01)(−0.02).We use this capability to study hyperfine-state-dependent collisions of Rb and Cs in the combined tweezer and compare the measured two-body loss rates with coupled-channel quantum scattering calculations

Two-photon photoassociation spectroscopy of CsYb: Ground-state interaction potential and interspecies scattering lengths

We perform two-photon photoassociation spectroscopy of the heteronuclear CsYb molecule to measure the binding energies of near-threshold vibrational levels of the X 2+ 1/2 molecular ground state. We report results for 133Cs170Yb, 133Cs173Yb, and 133Cs174Yb, in each case determining the energy of several vibrational levels including the least-bound state. We fit an interaction potential based on electronic structure calculations to the binding energies for all three isotopologs and find that the ground-state potential supports 77 vibrational levels. We use the fitted potential to predict the interspecies s-wave scattering lengths for all seven Cs+Yb isotopic mixtures

Observation of magnetic Feshbach resonances between Cs and 173Yb

We report the observation of magnetic Feshbach resonances between 173 Yb and 133 Cs . In a mixture of Cs atoms prepared in the ( f = 3 , m f = 3 ) state and unpolarized fermionic 173 Yb , we observe resonant atom loss due to two sets of magnetic Feshbach resonances around 622 and 702 G. Resonances for individual Yb nuclear spin components m i , Yb are split by its interaction with the Cs electronic spin, which also provides the main coupling mechanism for the observed resonances. The observed splittings and relative resonance strengths are in good agreement with theoretical predictions from coupled-channel calculations

Formation of Ultracold Molecules by Merging Optical Tweezers

We demonstrate the formation of a single RbCs molecule during the merging of two optical tweezers, one containing a single Rb atom and the other a single Cs atom. Both atoms are initially predominantly in the motional ground states of their respective tweezers. We confirm molecule formation and establish the state of the molecule formed by measuring its binding energy. We find that the probability of molecule formation can be controlled by tuning the confinement of the traps during the merging process, in good agreement with coupled-channel calculations. We show that the conversion efficiency from atoms to molecules using this technique is comparable to magnetoassociation

Improvement of cardiac contractile function by peptide-based inhibition of NF-κB in the utrophin/dystrophin-deficient murine model of muscular dystrophy

<p>Abstract</p> <p>Background</p> <p>Duchenne muscular dystrophy (DMD) is an inherited and progressive disease causing striated muscle deterioration. Patients in their twenties generally die from either respiratory or cardiac failure. In order to improve the lifespan and quality of life of DMD patients, it is important to prevent or reverse the progressive loss of contractile function of the heart. Recent studies by our labs have shown that the peptide NBD (Nemo Binding Domain), targeted at blunting Nuclear Factor κB (NF-κB) signaling, reduces inflammation, enhances myofiber regeneration, and improves contractile deficits in the diaphragm in dystrophin-deficient <it>mdx </it>mice.</p> <p>Methods</p> <p>To assess whether cardiac function in addition to diaphragm function can be improved, we investigated physiological and histological parameters of cardiac muscle in mice deficient for both dystrophin and its homolog utrophin (double knockout = dko) mice treated with NBD peptide. These dko mice show classic pathophysiological hallmarks of heart failure, including myocyte degeneration, an impaired force-frequency response and a severely blunted β-adrenergic response. Cardiac contractile function at baseline and frequencies and pre-loads throughout the in vivo range as well as β-adrenergic reserve was measured in isolated cardiac muscle preparations. In addition, we studied histopathological and inflammatory markers in these mice.</p> <p>Results</p> <p>At baseline conditions, active force development in cardiac muscles from NBD treated dko mice was more than double that of vehicle-treated dko mice. NBD treatment also significantly improved frequency-dependent behavior of the muscles. The increase in force in NBD-treated dko muscles to β-adrenergic stimulation was robustly restored compared to vehicle-treated mice. However, histological features, including collagen content and inflammatory markers were not significantly different between NBD-treated and vehicle-treated dko mice.</p> <p>Conclusions</p> <p>We conclude that NBD can significantly improve cardiac contractile dysfunction in the dko mouse model of DMD and may thus provide a novel therapeutic treatment for heart failure.</p

HFE mutations, iron deficiency and overload in 10 500 blood donors

People with genetic haemochromatosis (GH) accumulate iron from excessive dietary absorption. In populations of northern European origin, over 90% of patients are homozygous for the C282Y mutation of the HFE gene. While about 1 in 200 people in the general population have this genotype the proportion who develop clinical haemochromatosis is not known. The influence of HFE genotype on iron status was investigated in 10 556 blood donors. The allele frequencies of the C282Y and H63D mutations were

Dystrophin glycoprotein complex dysfunction:a regulatory link between muscular dystrophy and cancer cachexia

SummaryCachexia contributes to nearly a third of all cancer deaths, yet the mechanisms underlying skeletal muscle wasting in this syndrome remain poorly defined. We report that tumor-induced alterations in the muscular dystrophy-associated dystrophin glycoprotein complex (DGC) represent a key early event in cachexia. Muscles from tumor-bearing mice exhibited membrane abnormalities accompanied by reduced levels of dystrophin and increased glycosylation on DGC proteins. Wasting was accentuated in tumor mdx mice lacking a DGC but spared in dystrophin transgenic mice that blocked induction of muscle E3 ubiquitin ligases. Furthermore, DGC deregulation correlated positively with cachexia in patients with gastrointestinal cancers. Based on these results, we propose that, similar to muscular dystrophy, DGC dysfunction plays a critical role in cancer-induced wasting