297 research outputs found

    Using a quitline plus low-cost nicotine replacement therapy to help disadvantaged smokers to quit

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    Objectives: To trial an intervention in a real-life setting to motivate low-income smokers to try to quit. The intervention under trial was the addition of subsidised nicotine replacement therapy (NRT) to a standard population quitline service. Design: Participants were low-income smokers, recruited ‘‘cold’’ via either a letter in the mail or a flyer inserted in a local newspaper. The intervention group received the usual service of multisession counselling from the quitline plus access to heavily subsidised NRT. A comparison group received the usual quitline service only. Participants were followed up at 3, 6, and 12 months. Trial participants were also compared with a sample of general callers to the quitline. Results: The offer of subsidised NRT recruited more than twice as many low-income smokers than the offer of the cessation service alone (intervention group n=1000;comparison group n=377). 63% were first-time callers to the quitline. Intervention respondents showed higher levels of nicotine dependence than comparison group respondents. Comparisons of quitting data were confounded by the differences in the respondents at baseline. 73.5% of smokers in the intervention group tried to quit compared to 61.0% in the comparison group. Unadjusted quit rates were higher in the intervention group than in the comparison group at 3 months and 6 months but not at 12 months. Conclusions: Disadvantaged smokers were easily engaged to call the quitline, particularly when offered subsidised NRT. Disadvantaged smokers using the quitline, with and without subsidised NRT, achieved cessation outcomes comparable to other studies of ‘‘mainstream’’ smokers.C L Miller and V Sediv

    Networks from gene expression time series: characterization of correlation patterns

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    This paper describes characteristic features of networks reconstructed from gene expression time series data. Several null models are considered in order to discriminate between informations embedded in the network that are related to real data, and features that are due to the method used for network reconstruction (time correlation).Comment: 10 pages, 3 BMP figures, 1 Table. To appear in Int. J. Bif. Chaos, July 2007, Volume 17, Issue

    ELF3 controls thermoresponsive growth in Arabidopsis

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    Plant development is highly responsive to ambient temperature, and this trait has been linked to the ability of plants to adapt to climate change [1]. The mechanisms by which natural populations modulate their thermoresponsiveness are not known [2]. To address this, we surveyed Arabidopsis accessions for variation in thermal responsiveness of elongation growth and mapped the corresponding loci. We find that the transcriptional regulator EARLY FLOWERING3 (ELF3) controls elongation growth in response to temperature. Through a combination of modeling and experiments, we show that high temperature relieves the gating of growth at night, highlighting the importance of temperature-dependent repressors of growth. ELF3 gating of transcriptional targets responds rapidly and reversibly to changes in temperature. We show that the binding of ELF3 to target promoters is temperature dependent, suggesting a mechanism where temperature directly controls ELF3 activity

    Correlation analysis reveals the emergence of coherence in the gene expression dynamics following system perturbation

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    Time course gene expression experiments are a popular means to infer co-expression. Many methods have been proposed to cluster genes or to build networks based on similarity measures of their expression dynamics. In this paper we apply a correlation based approach to network reconstruction to three datasets of time series gene expression following system perturbation: 1) Conditional, Tamoxifen dependent, activation of the cMyc proto-oncogene in rat fibroblast; 2) Genomic response to nutrition changes in D. melanogaster; 3) Patterns of gene activity as a consequence of ageing occurring over a life-span time series (25y–90y) sampled from T-cells of human donors

    Time-domain characterization and correction of on-chip distortion of control pulses in a quantum processor

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    We introduce Cryoscope, a method for sampling on-chip baseband pulses used to dynamically control qubit frequency in a quantum processor. We specifically use Cryoscope to measure the step response of the dedicated flux control lines of two-junction transmon qubits in circuit QED processors with the temporal resolution of the room-temperature arbitrary waveform generator producing the control pulses. As a first application, we iteratively improve this step response using optimized real-time digital filters to counter the linear-dynamical distortion in the control line, as needed for high-fidelity, repeatable one- and two-qubit gates based on dynamical control of qubit frequency

    Myc Inhibits p27-Induced Erythroid Differentiation of Leukemia Cells by Repressing Erythroid Master Genes without Reversing p27-Mediated Cell Cycle Arrest

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    Inhibition of differentiation has been proposed as an important mechanism for Myc-induced tumorigenesis, but the mechanisms involved are unclear. We have established a genetically defined differentiation model in human leukemia K562 cells by conditional expression of the cyclin-dependent kinase (Cdk) inhibitor p27 (inducible by Zn2+) and Myc (activatable by 4-hydroxy-tamoxifen). Induction of p27 resulted in erythroid differentiation, accompanied by Cdk inhibition and G1 arrest. Interestingly, activation of Myc inhibited p27-mediated erythroid differentiation without affecting p27-mediated proliferation arrest. Microarray-based gene expression indicated that, in the presence of p27, Myc blocked the upregulation of several erythroid-cell-specific genes, including NFE2, JUNB, and GATA1 (transcription factors with a pivotal role in erythropoiesis). Moreover, Myc also blocked the upregulation of Mad1, a transcriptional antagonist of Myc that is able to induce erythroid differentiation. Cotransfection experiments demonstrated that Myc-mediated inhibition of differentiation is partly dependent on the repression of Mad1 and GATA1. In conclusion, this model demonstrates that Myc-mediated inhibition of differentiation depends on the regulation of a specific gene program, whereas it is independent of p27-mediated cell cycle arrest. Our results support the hypothesis that differentiation inhibition is an important Myc tumorigenic mechanism that is independent of cell proliferation. Copyright © 2008, American Society for Microbiology. All Rights Reserved.This study was supported by grants CICYT SAF05-00461 from the Spanish Ministerio de Educación y Ciencia (MEC), ISCIII-RETIC RD06/0020 from the Spanish Ministerio de Sanidad y Consumo, API-17-05 from the Fundación Marques de Valdecilla (to J.L), and FIS04/1083 (to M.D.D). J.C.A., G.B., and N.F. were supported by fellowships from the MEC, and V.T. was supported by a Lady Tata Memorial Trust award.Peer Reviewe
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