Efficient Production of Large 39K Bose-Einstein Condensates

We describe an experimental setup and the cooling procedure for producing 39K Bose-Einstein condensates of over 4x10^5 atoms. Condensation is achieved via a combination of sympathetic cooling with 87Rb in a quadrupole-Ioffe-configuration (QUIC) magnetic trap, and direct evaporation in a large volume crossed optical dipole trap, where we exploit the broad Feshbach resonance at 402 G to tune the 39K interactions from weak and attractive to strong and repulsive. In the same apparatus we create quasi-pure 87Rb condensates of over 8x10^5 atoms.Comment: 7 pages, 5 figures; figure font compatibility improve

Can a Bose gas be saturated?

Bose-Einstein condensation is unique among phase transitions between different states of matter in the sense that it occurs even in the absence of interactions between particles. In Einstein's textbook picture of an ideal gas, purely statistical arguments set an upper bound on the number of particles occupying the excited states of the system, and condensation is driven by this saturation of the quantum vapour. Dilute ultracold atomic gases are celebrated as a realisation of Bose-Einstein condensation in close to its purely statistical form. Here we scrutinise this point of view using an ultracold gas of potassium (39K) atoms, in which the strength of interactions can be tuned via a Feshbach scattering resonance. We first show that under typical experi-mental conditions a partially condensed atomic gas strongly deviates from the textbook concept of a saturated vapour. We then use measurements at a range of interaction strengths and temperatures to extrapolate to the non-interacting limit, and prove that in this limit the behaviour of a Bose gas is consistent with the saturation picture. Finally, we provide evidence for the universality of our observations through additional measurements with a different atomic species, 87Rb. Our results suggest a new way of characterising condensation phenomena in different physical systems.Comment: 6 pages, 5 figure

Condensation dynamics in a quantum-quenched Bose gas

By quenching the strength of interactions in a partially condensed Bose gas we create a "super-saturated" vapor which has more thermal atoms than it can contain in equilibrium. Subsequently, the number of condensed atoms ($N_0$) grows even though the temperature ($T$) rises and the total atom number decays. We show that the non-equilibrium evolution of the system is isoenergetic and for small initial $N_0$ observe a clear separation between $T$ and $N_0$ dynamics, thus explicitly demonstrating the theoretically expected "two-step" picture of condensate growth. For increasing initial $N_0$ values we observe a crossover to classical relaxation dynamics. The size of the observed quench-induced effects can be explained using a simple equation of state for an interacting harmonically-trapped atomic gas.Comment: 4 pages, 4 figure

Excitotoxicity Triggered by Neurobasal Culture Medium

Neurobasal defined culture medium has been optimized for survival of rat embryonic hippocampal neurons and is now widely used for many types of primary neuronal cell culture. Therefore, we were surprised that routine medium exchange with serum- and supplement-free Neurobasal killed as many as 50% of postnatal hippocampal neurons after a 4 h exposure at day in vitro 12–15. Minimal Essential Medium (MEM), in contrast, produced no significant toxicity. Detectable Neurobasal-induced neuronal death occurred with as little as 5 min exposure, measured 24 h later. D-2-Amino-5-phosphonovalerate (D-APV) completely prevented Neurobasal toxicity, implicating direct or indirect N-methyl-D-aspartate (NMDA) receptor-mediated neuronal excitotoxicity. Whole-cell recordings revealed that Neurobasal but not MEM directly activated D-APV-sensitive currents similar in amplitude to those gated by 1 µM glutamate. We hypothesized that L-cysteine likely mediates the excitotoxic effects of Neurobasal incubation. Although the original published formulation of Neurobasal contained only 10 µM L-cysteine, commercial recipes contain 260 µM, a concentration in the range reported to activate NMDA receptors. Consistent with our hypothesis, 260 µM L-cysteine in bicarbonate-buffered saline gated NMDA receptor currents and produced toxicity equivalent to Neurobasal. Although NMDA receptor-mediated depolarization and Ca2+ influx may support survival of young neurons, NMDA receptor agonist effects on development and survival should be considered when employing Neurobasal culture medium

Bypassing cellular EGF receptor dependence through epithelial-to-mesenchymal-like transitions

Over 90% of all cancers are carcinomas, malignancies derived from cells of epithelial origin. As carcinomas progress, these tumors may lose epithelial morphology and acquire mesenchymal characteristics which contribute to metastatic potential. An epithelial-to-mesenchymal transition (EMT) similar to the process critical for embryonic development is thought to be an important mechanism for promoting cancer invasion and metastasis. Epithelial-to-mesenchymal transitions have been induced in vitro by transient or unregulated activation of receptor tyrosine kinase signaling pathways, oncogene signaling and disruption of homotypic cell adhesion. These cellular models attempt to mimic the complexity of human carcinomas which respond to autocrine and paracrine signals from both the tumor and its microenvironment. Activation of the epidermal growth factor receptor (EGFR) has been implicated in the neoplastic transformation of solid tumors and overexpression of EGFR has been shown to correlate with poor survival. Notably, epithelial tumor cells have been shown to be significantly more sensitive to EGFR inhibitors than tumor cells which have undergone an EMT-like transition and acquired mesenchymal characteristics, including non-small cell lung (NSCLC), head and neck (HN), bladder, colorectal, pancreas and breast carcinomas. EGFR blockade has also been shown to inhibit cellular migration, suggesting a role for EGFR inhibitors in the control of metastasis. The interaction between EGFR and the multiple signaling nodes which regulate EMT suggest that the combination of an EGFR inhibitor and other molecular targeted agents may offer a novel approach to controlling metastasis