Spinor Dynamics-Driven Formation of a Dual-Beam Atom Laser

We demonstrate a novel dual-beam atom laser formed by outcoupling oppositely polarized components of an F=1 spinor Bose-Einstein condensate whose Zeeman sublevel populations have been coherently evolved through spin dynamics. The condensate is formed through all-optical means using a single-beam running-wave dipole trap. We create a condensate in the field-insensitive $m_F=0$ state, and drive coherent spin-mixing evolution through adiabatic compression of the initially weak trap. Such dual beams, number-correlated through the angular momentum-conserving reaction $2m_0\leftrightharpoons m_{+1}+m_{-1}$, have been proposed as tools to explore entanglement and squeezing in Bose-Einstein condensates, and have potential use in precision phase measurements.Comment: 4 pages, 4 figure

Differential Light Shift Cancellation in a Magnetic-Field-Insensitive Transition of 87^{87}Rb

We demonstrate near-complete cancellation of the differential light shift of a two-photon magnetic-field-insensitive microwave hyperfine (clock) transition in $^{87}$Rb atoms trapped in an optical lattice. Up to $95(2)$ of the differential light shift is canceled while maintaining magnetic-field insensitivity. This technique should have applications in quantum information and frequency metrology.Comment: 5 pages, 4 figure

Observation of ultracold atomic bubbles in orbital microgravity

Substantial leaps in the understanding of quantum systems have been driven by exploring geometry, topology, dimensionality and interactions in ultracold atomic ensembles1–6. A system where atoms evolve while confined on an ellipsoidal surface represents a heretofore unexplored geometry and topology. Realizing an ultracold bubble—potentially Bose–Einstein condensed—relates to areas of interest including quantized-vortex flow constrained to a closed surface topology, collective modes and self-interference via bubble expansion7–17. Large ultracold bubbles, created by inflating smaller condensates, directly tie into Hubble-analogue expansion physics18–20. Here we report observations from the NASA Cold Atom Lab21 facility onboard the International Space Station of bubbles of ultracold atoms created using a radiofrequency-dressing protocol. We observe bubble configurations of varying size and initial temperature, and explore bubble thermodynamics, demonstrating substantial cooling associated with inflation. We achieve partial coverings of bubble traps greater than one millimetre in size with ultracold films of inferred few-micrometre thickness, and we observe the dynamics of shell structures projected into free-evolving harmonic confinement. The observations are among the first measurements made with ultracold atoms in space, using perpetual freefall to explore quantum systems that are prohibitively difficult to create on Earth. This work heralds future studies (in orbital microgravity) of the Bose–Einstein condensed bubble, the character of its excitations and the role of topology in its evolution

Shell potentials for microgravity Bose-Einstein condensates

Extending the understanding of Bose-Einstein condensate (BEC) physics to new geometries and topologies has a long and varied history in ultracold atomic physics. One such new geometry is that of a bubble, where a condensate would be confined to the surface of an ellipsoidal shell. Study of this geometry would give insight into new collective modes, self-interference effects, topology-dependent vortex behavior, dimensionality crossovers from thick to thin shells, and the properties of condensates pushed into the ultradilute limit. Here we discuss a proposal to implement a realistic experimental framework for generating shell-geometry BEC using radiofrequency dressing of magnetically-trapped samples. Such a tantalizing state of matter is inaccessible terrestrially due to the distorting effect of gravity on experimentally-feasible shell potentials. The debut of an orbital BEC machine (NASA Cold Atom Laboratory, aboard the International Space Station) has enabled the operation of quantum-gas experiments in a regime of perpetual freefall, and thus has permitted the planning of microgravity shell-geometry BEC experiments. We discuss specific experimental configurations, applicable inhomogeneities and other experimental challenges, and outline potential experiments.Comment: 6 pages, 3 figure

Exploring the limits of ultracold atoms in space

Existing space-based cold atom experiments have demonstrated the utility of microgravity for improvements in observation times and for minimizing the expansion energy and rate of a freely evolving coherent matter wave. In this paper we explore the potential for space-based experiments to extend the limits of ultracold atoms utilizing not just microgravity, but also other aspects of the space environment such as exceptionally good vacuums and extremely cold temperatures. The tantalizing possibility that such experiments may one day be able to probe physics of quantum objects with masses approaching the Planck mass is discussed

Tonic and Phasic Amperometric Monitoring of Dopamine Using Microelectrode Arrays in Rat Striatum

Here we report a novel microelectrode array recording approach to measure tonic (resting) and phasic release of dopamine (DA) in DA-rich areas such as the rat striatum and nucleus accumbens. The resulting method is tested in intact central nervous system (CNS) and in animals with extensive loss of the DA pathway using the neurotoxin, 6-hydroxyDA (6-OHDA). The self-referencing amperometric recording method employs Nafion-coated with and without m-phenylenediamine recording sites that through real-time subtraction allow for simultaneous measures of tonic DA levels and transient changes due to depolarization and amphetamine-induced release. The recording method achieves low-level measures of both tonic and phasic DA with decreased recording drift allowing for enhanced sensitivity normally not achieved with electrochemical sensors in vivo

The reaction of bovine alpha-thrombin with tetranitromethane. Characterization of the modified protein.

Previous studies from several laboratories have shown that thrombin is inactivated by tetranitromethane with the formation of nitrotyrosine. The inactivation is characterized by an apparently greater loss of fibrinogen-clotting activity than activity toward synthetic ester substrates, suggesting that the residues modified by tetranitromethane are involved in the interaction of thrombin with fibrinogen. This study was designed 1) to determine the effect of solvent conditions on the rate of modification and the stoichiometry of the reaction of tetranitromethane with bovine alpha-thrombin; 2) to identify the residue(s) modified; and 3) to characterize the modified enzyme with respect to its interaction with peptide nitroanilide substrates and fibrinogen. The inactivation of thrombin by tetranitromethane proceeded more rapidly in 50 mM Tris, pH 8.0, than in 50 mM sodium phosphate, 100 mM NaCl, pH 8.0. Approximately 10% fibrinogen-clotting activity remained at maximal inactivation. A study of the effect of tetranitromethane concentration on the rate of inactivation suggested that the loss of activity was the result of the modification of 1 mol of tyrosine/mol of thrombin. A similar result was obtained from the analysis of the extent of inactivation as a function of the extent of protein modification. Structural analysis of the modified protein showed substantial modification at both Tyr71 and Tyr85. Enzyme kinetic studies were performed with the modified protein and a control thrombin with N2-tosylglycylprolylarginine p-nitroanilide. H-D-phenylalanylpipecolylarginine p-nitronailide, and purified bovine fibrinogen. With all three substrates, a substantial decrease in kcat was observed, whereas there was essentially no change in Km. These results suggest that, contrary to previous suggestions, the modification of Tyr71 and Tyr85 in thrombin does not influence the binding of substrates, but rather influences active site reactivity

The Endogenous Th17 Response in NO<inf>2</inf>-Promoted Allergic Airway Disease Is Dispensable for Airway Hyperresponsiveness and Distinct from Th17 Adoptive Transfer

Severe, glucocorticoid-resistant asthma comprises 5-7% of patients with asthma. IL-17 is a biomarker of severe asthma, and the adoptive transfer of Th17 cells in mice is sufficient to induce glucocorticoid-resistant allergic airway disease. Nitrogen dioxide (NO2) is an environmental toxin that correlates with asthma severity, exacerbation, and risk of adverse outcomes. Mice that are allergically sensitized to the antigen ovalbumin by exposure to NO2 exhibit a mixed Th2/Th17 adaptive immune response and eosinophil and neutrophil recruitment to the airway following antigen challenge, a phenotype reminiscent of severe clinical asthma. Because IL-1 receptor (IL-1R) signaling is critical in the generation of the Th17 response in vivo, we hypothesized that the IL-1R/Th17 axis contributes to pulmonary inflammation and airway hyperresponsiveness (AHR) in NO2-promoted allergic airway disease and manifests in glucocorticoid-resistant cytokine production. IL-17A neutralization at the time of antigen challenge or genetic deficiency in IL-1R resulted in decreased neutrophil recruitment to the airway following antigen challenge but did not protect against the development of AHR. Instead, IL-1R-/- mice developed exacerbated AHR compared to WT mice. Lung cells from NO2-allergically inflamed mice that were treated in vitro with dexamethasone (Dex) during antigen restimulation exhibited reduced Th17 cytokine production, whereas Th17 cytokine production by lung cells from recipient mice of in vitro Th17-polarized OTII T-cells was resistant to Dex. These results demonstrate that the IL-1R/Th17 axis does not contribute to AHR development in NO2-promoted allergic airway disease, that Th17 adoptive transfer does not necessarily reflect an endogenously-generated Th17 response, and that functions of Th17 responses are contingent on the experimental conditions in which they are generated. © 2013 Martin et al

Evidence for a prevalent dimorphism in the activation peptide of human coagulation factor IX.

We have independently isolated and characterized cDNA and genomic clones for the human coagulation factor IX. Sequence analysis in both cases indicates that threonine is encoded by the triplet ACT as the third residue of the activation peptide. This is in agreement with some earlier reports but in disagreement with others that show the alanine triplet GCT at this position. The discrepancy can thus be accounted for by natural variation of a single nucleotide in the normal population. Amino acid sequence analyses of activated factor IX from plasma samples of four individuals yielded two cases of alanine and two cases of threonine at the third position of the activation peptide. In factor IX from pooled plasma and in factor IX from a heterozygous individual, however, both alanine and threonine were found. Taken together, the findings show that a prevalent nondeleterious dimorphism exists in the activation peptide of human coagulation factor IX

The effect of cigarette smoke exposure on the development of inflammation in lungs, gut and joints of TNFΔARE mice

The inflammatory cytokine TNF-alpha is a central mediator in many immune-mediated diseases, such as Crohn's disease (CD), spondyloarthritis (SpA) and chronic obstructive pulmonary disease (COPD). Epidemiologic studies have shown that cigarette smoking (CS) is a prominent common risk factor in these TNF-dependent diseases. We exposed TNF Delta ARE mice; in which a systemic TNF-alpha overexpression leads to the development of inflammation; to 2 or 4 weeks of air or CS. We investigated the effect of deregulated TNF expression on CS-induced pulmonary inflammation and the effect of CS exposure on the initiation and progression of gut and joint inflammation. Upon 2 weeks of CS exposure, inflammation in lungs of TNF Delta ARE mice was significantly aggravated. However, upon 4 weeks of CS-exposure, this aggravation was no longer observed. TNF Delta ARE mice have no increases in CD4+ and CD8+ T cells and a diminished neutrophil response in the lungs after 4 weeks of CS exposure. In the gut and joints of TNF Delta ARE mice, 2 or 4 weeks of CS exposure did not modulate the development of inflammation. In conclusion, CS exposure does not modulate gut and joint inflammation in TNF Delta ARE mice. The lung responses towards CS in TNF Delta ARE mice however depend on the duration of CS exposure