259 research outputs found

    Cavity QED with a Bose-Einstein condensate

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    Cavity quantum electrodynamics (cavity QED) describes the coherent interaction between matter and an electromagnetic field confined within a resonator structure, and is providing a useful platform for developing concepts in quantum information processing. By using high-quality resonators, a strong coupling regime can be reached experimentally in which atoms coherently exchange a photon with a single light-field mode many times before dissipation sets in. This has led to fundamental studies with both microwave and optical resonators. To meet the challenges posed by quantum state engineering and quantum information processing, recent experiments have focused on laser cooling and trapping of atoms inside an optical cavity. However, the tremendous degree of control over atomic gases achieved with Bose-Einstein condensation has so far not been used for cavity QED. Here we achieve the strong coupling of a Bose-Einstein condensate to the quantized field of an ultrahigh-finesse optical cavity and present a measurement of its eigenenergy spectrum. This is a conceptually new regime of cavity QED, in which all atoms occupy a single mode of a matter-wave field and couple identically to the light field, sharing a single excitation. This opens possibilities ranging from quantum communication to a wealth of new phenomena that can be expected in the many-body physics of quantum gases with cavity-mediated interactions.Comment: 6 pages, 4 figures; version accepted for publication in Nature; updated Fig. 4; changed atom numbers due to new calibratio

    Flocked nasal swab versus nasopharyngeal aspirate for detection of respiratory tract viruses in immunocompromised adults: a matched comparative study

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    <p>Abstract</p> <p>Background</p> <p>Several studies have compared nasal swabs to the more invasive nasopharyngeal aspirate (NPA) for detection of respiratory viruses. Mostly, the comparisons have been performed on immunocompetent children with upper respiratory tract symptoms. The results range from a relatively poor sensitivity for the swabs to an even higher sensitivity than for the NPA. We aimed to investigate the sensitivity of a flocked nasal swab (fNS) on immunocompromised adults with febrile neutropenia.</p> <p>Methods</p> <p>During 16 months, adults with a hematological disorder presenting with febrile neutropenia were enrolled in the study. Paired samples of the fNS and NPA were collected in the outer part of the nasal cavity and the nasopharynx, respectively. The samples were analyzed regarding a panel of 15 respiratory viruses by means of quantitative polymerase chain reaction. Furthermore, as an indirect measure of cell yield by either method, the copy number of the human beta actin gene was also determined. Cohen's kappa was calculated as a measure of agreement of the results obtained from either method. Wilcoxon signed-rank test was used for comparison of cell yield.</p> <p>Results</p> <p>A total of 98 paired samples from a total of 89 patients were collected. Twenty of the pairs had virus detected in at least one of the specimens; 11 in both, 7 in NPA only, and 2 in fNS only. For the fNS, the overall sensitivity for any virus and for rhinovirus only was 65% and 78%, respectively. NPA was significantly superior to the fNS in collecting epithelial cells.</p> <p>Conclusion</p> <p>We found the overall sensitivity of 65% to be too low to replace NPA with this sampling technique in this patient category.</p

    A BCR-ABL Mutant Lacking Direct Binding Sites for the GRB2, CBL and CRKL Adapter Proteins Fails to Induce Leukemia in Mice

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    The BCR-ABL tyrosine kinase is the defining feature of chronic myeloid leukemia (CML) and its kinase activity is required for induction of this disease. Current thinking holds that BCR-ABL forms a multi-protein complex that incorporates several substrates and adaptor proteins and is stabilized by multiple direct and indirect interactions. Signaling output from this highly redundant network leads to cellular transformation. Proteins known to be associated with BCR-ABL in this complex include: GRB2, c-CBL, p62DOK, and CRKL. These proteins in turn, link BCR-ABL to various signaling pathways indicated in cellular transformation. In this study we show that a triple mutant of BCR-ABL with mutations of the direct binding sites for GRB2, CBL, p62DOK and CRKL, is defective for transformation of primary hematopoietic cells in vitro and in a murine CML model, while it retains the capacity to induce IL-3 independence in 32D cells. Compared to BCR-ABL, the triple mutant's ability to activate the MAP kinase and PI3-kinase pathways is severely compromised, while STAT5 phosphorylation is maintained, suggesting that the former are crucial for the transformation of primary cells, but dispensable for transformation of factor dependent cell lines. Our data suggest that inhibition of BCR-ABL-induced leukemia by disrupting protein interactions could be possible, but would require blocking of multiple sites

    Study protocol to investigate the effect of a lifestyle intervention on body weight, psychological health status and risk factors associated with disease recurrence in women recovering from breast cancer treatment

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    Background Breast cancer survivors often encounter physiological and psychological problems related to their diagnosis and treatment that can influence long-term prognosis. The aim of this research is to investigate the effects of a lifestyle intervention on body weight and psychological well-being in women recovering from breast cancer treatment, and to determine the relationship between changes in these variables and biomarkers associated with disease recurrence and survival. Methods/design Following ethical approval, a total of 100 patients will be randomly assigned to a lifestyle intervention (incorporating dietary energy restriction in conjunction with aerobic exercise training) or normal care control group. Patients randomised to the dietary and exercise intervention will be given individualised healthy eating dietary advice and written information and attend moderate intensity aerobic exercise sessions on three to five days per week for a period of 24 weeks. The aim of this strategy is to induce a steady weight loss of up to 0.5 Kg each week. In addition, the overall quality of the diet will be examined with a view to (i) reducing the dietary intake of fat to ~25% of the total calories, (ii) eating at least 5 portions of fruit and vegetables a day, (iii) increasing the intake of fibre and reducing refined carbohydrates, and (iv) taking moderate amounts of alcohol. Outcome measures will include body weight and body composition, psychological health status (stress and depression), cardiorespiratory fitness and quality of life. In addition, biomarkers associated with disease recurrence, including stress hormones, estrogen status, inflammatory markers and indices of innate and adaptive immune function will be monitored. Discussion This research will provide valuable information on the effectiveness of a practical, easily implemented lifestyle intervention for evoking positive effects on body weight and psychological well-being, two important factors that can influence long-term prognosis in breast cancer survivors. However, the added value of the study is that it will also evaluate the effects of the lifestyle intervention on a range of biomarkers associated with disease recurrence and survival. Considered together, the results should improve our understanding of the potential role that lifestyle-modifiable factors could play in saving or prolonging lives

    Phosphorylation of SOS1 on tyrosine 1196 promotes its RAC GEF activity and contributes to BCR-ABL leukemogenesis

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    Son of Sevenless 1 (SOS1) is a dual guanine nucleotide exchange factor (GEF) that activates the small GTPases RAC and RAS. Although the molecular mechanisms of RAS GEF catalysis have been unveiled, how SOS1 acquires RAC GEF activity and what is the physio-pathological relevance of this activity is much less understood. Here we show that SOS1 is tyrosine phosphorylated on Y1196 by ABL. Phosphorylation of Y1196 controls SOS1 inter-molecular interaction, is required to promote the exchange of nucleotides on RAC in vitro and for platelet-derived growth factor (PDGF) activation of RAC- and RAC-dependent actin remodeling and cell migration. SOS1 is also phosphorylated on Y1196 by BCR-ABL in chronic myelogenous leukemic cells. Importantly, in these cells, SOS1 is required for BCR-ABL-mediated activation of RAC, cell proliferation and transformation in vitro and in a xenograft mouse model. Finally, genetic removal of Sos1 in the bone marrow-derived cells (BMDCs) from Sos1fl/flmice and infected with BCR-ABL causes a significant delay in the onset of leukemogenesis once BMDCs are injected into recipient, lethally irradiated mice. Thus, SOS1 is required for full transformation and critically contribute to the leukemogenic potential of BCR-ABL

    Prioritizing sleep for healthy work schedules

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    Good sleep is advantageous to the quality of life. Sleep-related benefits are particularly helpful for the working class, since poor or inadequate amounts of sleep degrade work productivity and overall health. This review paper explores the essential role of sleep in healthy work schedules and primarily focuses on the timing of sleep in relation to the work period (that is, before, during and after work). Data from laboratory, field and modeling studies indicate that consistent amounts of sleep prior to work are fundamental to improved performance and alertness in the workplace. In addition, planned naps taken during work maintain appropriate levels of waking function for both daytime and night-time work. Clearly, sufficient sleep after work is vital in promoting recovery from fatigue. Recent data also suggest that the time interval between shifts should be adjusted according to the biological timing of sleep. Although sleep is more likely to be replaced by job and other activities in the real life, research shows that it is worthwhile to revise the work schedules in order to optimize sleep before, sometime during and after the work period. Therefore, we suggest establishing work-sleep balance, similar to work-life balance, as a principle for designing and improving work schedules

    A measurement of the mean central optical depth of galaxy clusters via the pairwise kinematic Sunyaev-Zel'dovich effect with SPT-3G and DES

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    We infer the mean optical depth of a sample of optically-selected galaxy clusters from the Dark Energy Survey (DES) via the pairwise kinematic Sunyaev-Zel'dovich (kSZ) effect. The pairwise kSZ signal between pairs of clusters drawn from the DES Year-3 cluster catalog is detected at 4.1σ4.1 \sigma in cosmic microwave background (CMB) temperature maps from two years of observations with the SPT-3G camera on the South Pole Telescope. After cuts, there are 24,580 clusters in the ∼1,400\sim 1,400 deg2^2 of the southern sky observed by both experiments. We infer the mean optical depth of the cluster sample with two techniques. The optical depth inferred from the pairwise kSZ signal is τˉe=(2.97±0.73)×10−3\bar{\tau}_e = (2.97 \pm 0.73) \times 10^{-3}, while that inferred from the thermal SZ signal is τˉe=(2.51±0.55stat±0.15syst)×10−3\bar{\tau}_e = (2.51 \pm 0.55^{\text{stat}} \pm 0.15^{\rm syst}) \times 10^{-3}. The two measures agree at 0.6σ0.6 \sigma. We perform a suite of systematic checks to test the robustness of the analysis

    Large intergenic non-coding RNA-RoR modulates reprogramming of human induced pluripotent stem cells

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    February 17, 2011The conversion of lineage-committed cells to induced pluripotent stem cells (iPSCs) by reprogramming is accompanied by a global remodeling of the epigenome[superscript 1, 2, 3, 4, 5], resulting in altered patterns of gene expression[superscript 2, 6, 7, 8, 9]. Here we characterize the transcriptional reorganization of large intergenic non-coding RNAs (lincRNAs)[superscript 10, 11] that occurs upon derivation of human iPSCs and identify numerous lincRNAs whose expression is linked to pluripotency. Among these, we defined ten lincRNAs whose expression was elevated in iPSCs compared with embryonic stem cells, suggesting that their activation may promote the emergence of iPSCs. Supporting this, our results indicate that these lincRNAs are direct targets of key pluripotency transcription factors. Using loss-of-function and gain-of-function approaches, we found that one such lincRNA (lincRNA-RoR) modulates reprogramming, thus providing a first demonstration for critical functions of lincRNAs in the derivation of pluripotent stem cells
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