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

Atoms in a radiofrequency-dressed optical lattice

We load cold atoms into an optical lattice dramatically reshaped by radiofrequency (rf) coupling of state-dependent lattice potentials. This rf dressing changes the unit cell of the lattice at a subwavelength scale, such that its curvature and topology departs strongly from that of a simple sinusoidal lattice potential. Radiofrequency dressing has previously been performed at length scales from mm to tens of microns, but not at the single-optical-wavelength scale. At this length scale significant coupling between adiabatic potentials leads to nonadiabatic transitions, which we measure as a function of lattice depth and dressing frequency and amplitude. We also investigate the dressing by measuring changes in the momentum distribution of the dressed states.Comment: 5 pages, 4 figure

Telomerase activity in human leukemic cells with or without monosomy 7 or 7q-

BACKGROUND: In bone marrow material from patients with various leukemias we noted that samples with either a deletion on the long arm of one chromosome 7 (7q-) or a monosomy 7 had a higher telomerase activity. Considering that introduction of a chromosome 7 into a cancer cell line had been reported to eliminate telomerase activity, that 7q- is a common negative prognostic finding in cancers, and that the deleted segment (band 7q31) contains an unidentified tumor suppressor gene, we wondered if this gene might be a telomerase inhibitor. RESULTS: We found no significant difference in telomerase activity between the three groups of patient samples. In contrast to reports on tumor cell lines we observed no amplification of the telomerase genes. METHODS: We analyzed telomerase activity and copy number of the telomerase genes hTERT and hTR in frozen archival bone marrow samples from leukemia patients with a referral diagnosis of AML, and either a monosomy for chromosome 7, a deletion on the long arm of chromosome 7 (7q-), or none of these aberrations. Telomerase activity was measured with a commercially available kit, and the copy number of the telomerase genes was tested by FISH. CONCLUSIONS: We found no evidence of a telomerase inhibitor in band 7q31. The lack of telomerase gene amplification found in cell lines from solid tumors could reflect that this amplification is a property of solid tumors, not of hematological cancers

Field-sensitive addressing and control of field-insensitive neutral-atom qubits

The establishment of a scalable scheme for quantum computing with addressable and long-lived qubits would be a scientific watershed, harnessing the laws of quantum physics to solve classically intractable problems. The design of many proposed quantum computational platforms is driven by competing needs: isolating the quantum system from the environment to prevent decoherence, and easily and accurately controlling the system with external fields. For example, neutral-atom optical-lattice architectures provide environmental isolation through the use of states that are robust against fluctuating external fields, yet external fields are essential for qubit addressing. Here we demonstrate the selection of individual qubits with external fields, despite the fact that the qubits are in field-insensitive superpositions. We use a spatially inhomogeneous external field to map selected qubits to a different field-insensitive superposition ("optical MRI"), minimally perturbing unselected qubits, despite the fact that the addressing field is not spatially localized. We show robust single-qubit rotations on neutral-atom qubits located at selected lattice sites. This precise coherent control is an important step forward for lattice-based neutral-atom quantum computation, and is quite generally applicable to state transfer and qubit isolation in other architectures using field-insensitive qubits.Comment: press embarg

Quantum computing implementations with neutral particles

We review quantum information processing with cold neutral particles, that is, atoms or polar molecules. First, we analyze the best suited degrees of freedom of these particles for storing quantum information, and then we discuss both single- and two-qubit gate implementations. We focus our discussion mainly on collisional quantum gates, which are best suited for atom-chip-like devices, as well as on gate proposals conceived for optical lattices. Additionally, we analyze schemes both for cold atoms confined in optical cavities and hybrid approaches to entanglement generation, and we show how optimal control theory might be a powerful tool to enhance the speed up of the gate operations as well as to achieve high fidelities required for fault tolerant quantum computation.Comment: 19 pages, 12 figures; From the issue entitled "Special Issue on Neutral Particles

Localization of telomeres and telomere-associated proteins in telomerase-negative Saccharomyces cerevisiae

Cells lacking telomerase cannot maintain their telomeres and undergo a telomere erosion phase leading to senescence and crisis in which most cells become nonviable. On rare occasions survivors emerge from these cultures that maintain their telomeres in alternative ways. The movement of five marked telomeres in Saccharomyces cerevisiae was followed in wild-type cells and through erosion, senescence/crisis and eventual survival in telomerase-negative (est2::HYG) yeast cells. It was found that during erosion, movements of telomeres in est2::HYG cells were indistinguishable from wild-type telomere movements. At senescence/crisis, however, most cells were in G2 arrest and the nucleus and telomeres traversed back and forth across the bud neck, presumably until cell death. Type I survivors, using subtelomeric Y′ amplification for telomere maintenance, continued to show this aberrant telomere movement. However, Type II survivors, maintaining telomeres by a sudden elongation of the telomere repeats, became indistinguishable from wild-type cells, consistent with growth properties of the two types of survivors. When telomere-associated proteins Sir2p, Sir3p and Rap1p were tagged, the same general trend was seen—Type I survivors retained the senescence/crisis state of protein localization, while Type II survivors were restored to wild type

Telomerase activity in melanoma and non-melanoma skin cancer

Telomeres are specialized structures consisting of repeat arrays of TTAGGGn located at the ends of chromosomes. They are essential for chromosome stability and, in the majority of normal somatic cells, telomeres shorten with each cell division. Most immortalized cell lines and tumours reactivate telomerase to stabilize the shortening chromosomes. Telomerase activation is regarded as a central step in carcinogenesis and, here, we demonstrate telomerase activation in premalignant skin lesions and also in all forms of skin cancer. Telomerase activation in normal skin was a rare event, and among 16 samples of normal skin (one with a history of chronic sun exposure) 12.5% (2 out of 16) exhibited telomerase activity. One out of 16 (6.25%) benign proliferative lesions, including viral and seborrhoeic wart samples, had telomerase activity. In premalignant actinic keratoses and Bowen's disease, 42% (11 out of 26) of samples exhibited telomerase activity. In the basal cell carcinoma and cutaneous malignant melanoma (CMM) lesions, telomerase was activated in 77% (10 out of 13) and 69% (22 out of 32) respectively. However, only 25% (3 out of 12) of squamous cell carcinomas (SCC) had telomerase activity. With the exception of one SCC sample, telomerase activity in a positive control cell line derived from a fibrosarcoma (HT1080) was not inhibited when mixed with the telomerase-negative SCC or CMM extracts, indicating that, overall, Taq polymerase and telomerase inhibitors were not responsible for the negative results. Mean telomere hybridizing restriction fragment (TRF) analysis was performed in a number of telomerase-positive and -negative samples and, although a broad range of TRF sizes ranging from 3.6 to 17 kb was observed, a relationship between telomerase status and TRF size was not found

A new shape for an old function: lasting effect of a physiologic surgical restoration of the left ventricle

BACKGROUND: Long-term morphofunctional outcome may vary widely in surgical anterior left ventricular wall restoration, suggesting variability in post-surgical remodeling similar to that observed following acute myocardial infarction. The aim of this pilot study was to demonstrate that surgical restoration obtained with a particular shape of endoventricular patch leads to steady morphofunctional ventricular improvement when geometry, volume and residual akinesia can be restored as normal as possible. METHODS: This study involved 12 consecutive patients with previous anterior myocardial infarction, dilated cardiomyopathy and no mitral procedures, who underwent left ventricular reconstruction and coronary revascularization between May 2002 and May 2003 using a small, narrow, oval patch aiming at a volume ≤ 45 mL/m(2 )with elliptical shape. Eleven geometric parameters were examined preoperatively and at least 3, 12 and 24 months after the operation by serial echocardiographic studies and evaluated by paired t test taking the time of surgery as a starting point for remodeling. RESULTS: All patients were in NYHA class 1 at follow-up. Patch geometry obtained a conical shape of the ventricle with new apex, physiologic rearrangement of functioning myocardial wall and small residual akinesia. Ventricular changes at the four time-points showed that all parameters improved significantly compared to preoperative values (end-diastolic volume = 184.2 ± 23.9 vs 139.9 ± 22.0, p = 0.001; vs 151.0 ± 33.8, p = 0.06; vs 144.9 ± 34.0, p = 0.38; end-systolic volume = 125.7 ± 20.6 vs 75.2 ± 14.1, p = 0.001; vs 82.1 ± 23.9, p = 0,18; vs 77.1 ± 19.4, p = 0.41) without further changes during follow-up except for wall motion score index (2.0 ± 0.2 to 1.7 ± 0.2, to 1.4 ± 0.2, to 1.3 ± 0.2) and percentage of akinesia (30.4 ± 7.5 to 29.3 ± 4.2, to 19.8 ± 11.6, to 14.5 ± 7.2) which slowly and significantly improved suggesting a positive post-surgery remodeling. CONCLUSION: Ventricular reconstruction caring of physiological shape, volume, revascularization and residual akinesia obtained a steady geometry. Positive remodeling and equalization of geometrical outcome may persistently prevent long-term redilation