Experimental Realization of Quantum-Resonance Ratchets

Quantum-resonance ratchets associated with the periodically kicked particle are experimentally realized for the first time. This is achieved by using a Bose-Einstein condensate exposed to a pulsed standing light wave and prepared in an initial state differing from the usual plane wave. Both the standing-wave potential and the initial state have a point symmetry around some center and the ratchet arises from the non-coincidence of the two centers. The dependence of the directed quantum transport on the quasimomentum is studied. A detailed theoretical analysis is used to explain the experimental results.Comment: Accepted for publication in Physical Review Letters (November 2007

Exploring the phase space of the quantum delta kicked accelerator

We experimentally explore the underlying pseudo-classical phase space structure of the quantum delta kicked accelerator. This was achieved by exposing a Bose-Einstein condensate to the spatially corrugated potential created by pulses of an off-resonant standing light wave. For the first time quantum accelerator modes were realized in such a system. By utilizing the narrow momentum distribution of the condensate we were able to observe the discrete momentum state structure of a quantum accelerator mode and also to directly measure the size of the structures in the phase space.Comment: 4 pages, 5 figures, added 2 references and figures are modified to increase the readability, submitted to Phys. Rev. Let

Creation mechanism of quantum accelerator modes

We investigate the creation mechanism of quantum accelerator modes which are attributed to the existence of the stability islands in an underlying pseudoclassical phase space of the quantum delta-kicked accelerator. Quantum accelerator modes can be created by exposing a Bose-Einstein condensate to a pulsed standing light wave. We show that constructive interference between momentum states populated by the pulsed light determines the stability island’s existence in the underlying pseudoclassical phase space. We generalize this interference model to incorporate higher-order accelerator modes, showing that they are generated if the rephasing occurs after multiple pulses. The model is extended to predict the momentum structure of the quantum accelerator modes close to higher-order quantum resonances. These predictions are in good agreement with our experimental observations

Multiple micro-optical atom traps with a spherically aberrated laser beam

We report on the loading of atoms contained in a magneto-optic trap into multiple optical traps formed within the focused beam of a CO_{2} laser. We show that under certain circumstances it is possible to create a linear array of dipole traps with well separated maxima. This is achieved by focusing the laser beam through lenses uncorrected for spherical aberration. We demonstrate that the separation between the micro-traps can be varied, a property which may be useful in experiments which require the creation of entanglement between atoms in different micro-traps. We suggest other experiments where an array of these traps could be useful.Comment: 10 pages, 3 figure

The N-Terminal Domain of Y-Box Binding Protein-1 Induces Cell Cycle Arrest in G2/M Phase by Binding to Cyclin D1

Y-box binding protein YB-1 is a multifunctional protein involved in cell proliferation, regulation of transcription and translation. Our previous study indicated that disruption of one allele of Chk-YB-1b gene in DT-40 cells resulted in major defects in the cell cycle. The abnormalities seen in heterozygous mutants could be attributed to a dominant negative effect exerted by the disrupted YB-1 allele product. To test this hypothesis the N-terminal sequence of the YB-1 was fused with the third helix of antennapedia and the green fluorescent protein. These purified fusion proteins were introduced into rat hepatoma cells and their effect on cell proliferation was studied. Results indicate that the N-terminal 77 amino acid domain of the YB-1 protein induced the cells to arrest in G2/M phase of the cell cycle and undergo apoptosis. Additional deletion analysis indicated that as few as 26 amino acids of the N-terminus of YB-1 can cause these phenotypic changes. We further demonstrated that this N-terminal 77 amino acid domain of YB-1 sequesters cyclin D1 in the cytoplasm of cells at G2/M phase of cell cycle. We conclude that the N-terminal domain of YB-1 plays a major role in cell cycle progression through G2/M phase of cell cycle

Interaction of Hepatitis C Viral Proteins with Cellular Oncoproteins in the Induction of Liver Cancer

Hepatitis C virus infection is a major health problem all over the world. A large proportion of patients infected by HCV develop liver cirrhosis or cancer. However, the mechanism(s) remain to be elucidated. Since HCV does not carry any known oncogene, it is thought that interaction between virally encoded proteins and host proteins is responsible for carcinogenesis. Many crucial interactions between HCV-encoded proteins and host proteins have been reported. In this review we focus on the interaction of viral proteins with important regulators of cell cycle—oncoproteins YB-1, p53, and cyclin D1—which play a major role in cell proliferation, apoptosis, DNA repair, and genomic stability. Genetic variants of HCV accumulate in patients and alter these interactions of host cell proteins. It is a battle between the virus and host and the final outcome depends on the winner; if the host succeeds in clearing the virus the patient may not develop serious liver diseases. On the other hand, if the virus dominates by evolving quasispecies which code for altered proteins that interact differently with host proteins, or induce mutations in host protooncogenes, then the patient may develop liver cirrhosis and/or liver cancer.</jats:p