2,959 research outputs found

    Thermo-mechanical sensitivity calibration of nanotorsional magnetometers

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    We report on the fabrication of sensitive nanotorsional resonators, which can be utilized as magnetometers for investigating the magnetization dynamics in small magnetic elements. The thermo-mechanical noise is calibrated with the resonator displacement in order to determine the ultimate mechanical torque sensitivity of the magnetometer.Comment: 56th Annual Conference on Magnetism and Magnetic Material

    920-52 Are Provider Profiles Affected by Risk-adjustment Methodology? Results from the Cooperative Cardiovascular Project

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    Health care payors and consumers have a growing interest in risk-adjusted provider profiles. Using chart-abstracted clinical data from the Cooperative Cardiovascular Project, we ranked 28 hospitals performing bypass surgery in Alabama and Iowa by their risk-adjusted surgical mortality rates using three published risk-adjustment methodologies: Parsonnet (PI, O’Connor (a) and Hannan (H). In total. 3653 bypass surgery cases performed from 6/92 to 3/93 were reviewed (mean 130 cases/hospital). The discriminatory abilities of each method for predicting surgical mortality were quite similar (area under ROC curves 0.72–0.75). Below, we display the risk-adjusted hospital rankings (comparing observed with expected mortality) by these three riskadjustment techniques:In terms of hospital rankings, there was generally close correlation between any two of the methods (Spearman's R=0.87,0.88, and 0.93, comparing P-O, P-H, and H-O). Rankings for an individual hospital varied, however, an average of ±3.3 ranks (range 0–12 ranks) depending on which riskadjustment methodology was used.ConclusionIn general. published methods of risk-adjustment for bypass surgery accurately identify institutions with low, moderate and high adjusted mortality outcomes. The precise ranking of an individual hospital. however, may vary depending on the risk adjustment method applied

    Sentiment analysis with genetically evolved Gaussian kernels

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    Sentiment analysis consists of evaluating opinions or statements based on text analysis. Among the methods used to estimate the degree to which a text expresses a certain sentiment are those based on Gaussian Processes. However, traditional Gaussian Processes methods use a prede- fined kernels with hyperparameters that can be tuned but whose structure can not be adapted. In this paper, we propose the application of Genetic Programming for the evolution of Gaussian Process kernels that are more precise for sentiment analysis. We use use a very flexible representation of kernels combined with a multi-objective approach that considers si- multaneously two quality metrics and the computational time required to evaluate those kernels. Our results show that the algorithm can outper- form Gaussian Processes with traditional kernels for some of the sentiment analysis tasks considered

    Optimal learning rules for familiarity detection

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    It has been suggested that the mammalian memory system has both familiarity and recollection components. Recently, a high-capacity network to store familiarity has been proposed. Here we derive analytically the optimal learning rule for such a familiarity memory using a signalto- noise ratio analysis. We find that in the limit of large networks the covariance rule, known to be the optimal local, linear learning rule for pattern association, is also the optimal learning rule for familiarity discrimination. The capacity is independent of the sparseness of the patterns, as long as the patterns have a fixed number of bits set. The corresponding information capacity is 0.057 bits per synapse, less than typically found for associative networks

    Confirmation of double-peaked time distribution of mortality among Asian breast cancer patients in a population-based study

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    INTRODUCTION: Double-peaked time distributions of the mortality hazard function have been reported for breast cancer patients from Western populations treated with mastectomy alone. These are thought to reflect accelerated tumour growth at micrometastatic sites mediated by angiogenesis after primary tumour removal as well as tumor dormancy. Similar data are not available for Asian populations. We sought to investigate whether differences exist in the pattern of mortality hazard function between Western breast cancer patients and their Asian counterparts in Singapore, which may suggest underlying differences in tumor biology between the two populations. METHODS: We performed a retrospective cohort study of female unilateral breast cancer patients diagnosed in Singapore between October 1994 and June 1999. Data regarding patient demographics, tumour characteristics and death were available. Overall survival curves were calculated using the Kaplan-Meier method. The hazard rate was calculated as the conditional probability of dying in a time interval, given that the patient was alive at the beginning of the interval. The life table method was used to calculate the yearly hazard rates. RESULTS: In the 2,105 women identified, 956 patients (45.4%) had mastectomy alone. Demographic characteristics were as follows: 86.5% were Chinese, 45.2% were postmenopausal, 38.9% were hormone receptor positive, 54.6% were node negative and 44.1% had high histological grade. We observed a double-peaked mortality hazard pattern, with a first peak in mortality achieving its maximum between years 2 and 4 after mastectomy, and a second large peak in mortality during year 9. Analyses by subgroups revealed a similar pattern regardless of T stage, or node or menopausal status. This pattern was also noted in high-grade tumors but not in those that were well to moderately differentiated. The double-peaked pattern observed in Singaporean women was quantitatively and qualitatively similar to those reported in Western series. CONCLUSION: Our study confirms the existence of a double-peaked process in Asian patients, and it gives further support to the tumour dormancy hypothesis after mastectomy

    APAF1 is a key transcriptional target for p53 in the regulation of neuronal cell death

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    p53 is a transcriptional activator which has been implicated as a key regulator of neuronal cell death after acute injury. We have shown previously that p53-mediated neuronal cell death involves a Bax-dependent activation of caspase 3; however, the transcriptional targets involved in the regulation of this process have not been identified. In the present study, we demonstrate that p53 directly upregulates Apaf1 transcription as a critical step in the induction of neuronal cell death. Using DNA microarray analysis of total RNA isolated from neurons undergoing p53-induced apoptosis a 5–6-fold upregulation of Apaf1 mRNA was detected. Induction of neuronal cell death by camptothecin, a DNA-damaging agent that functions through a p53-dependent mechanism, resulted in increased Apaf1 mRNA in p53-positive, but not p53-deficient neurons. In both in vitro and in vivo neuronal cell death processes of p53-induced cell death, Apaf1 protein levels were increased. We addressed whether p53 directly regulates Apaf1 transcription via the two p53 consensus binding sites in the Apaf1 promoter. Electrophoretic mobility shift assays demonstrated p53–DNA binding activity at both p53 consensus binding sequences in extracts obtained from neurons undergoing p53-induced cell death, but not in healthy control cultures or when p53 or the p53 binding sites were inactivated by mutation. In transient transfections in a neuronal cell line with p53 and Apaf1 promoter–luciferase constructs, p53 directly activated the Apaf1 promoter via both p53 sites. The importance of Apaf1 as a p53 target gene in neuronal cell death was evaluated by examining p53-induced apoptotic pathways in primary cultures of Apaf1-deficient neurons. Neurons treated with camptothecin were significantly protected in the absence of Apaf1 relative to those derived from wild-type littermates. Together, these results demonstrate that Apaf1 is a key transcriptional target for p53 that plays a pivotal role in the regulation of apoptosis after neuronal injury

    First radial velocity results from the MINiature Exoplanet Radial Velocity Array (MINERVA)

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    The MINiature Exoplanet Radial Velocity Array (MINERVA) is a dedicated observatory of four 0.7m robotic telescopes fiber-fed to a KiwiSpec spectrograph. The MINERVA mission is to discover super-Earths in the habitable zones of nearby stars. This can be accomplished with MINERVA's unique combination of high precision and high cadence over long time periods. In this work, we detail changes to the MINERVA facility that have occurred since our previous paper. We then describe MINERVA's robotic control software, the process by which we perform 1D spectral extraction, and our forward modeling Doppler pipeline. In the process of improving our forward modeling procedure, we found that our spectrograph's intrinsic instrumental profile is stable for at least nine months. Because of that, we characterized our instrumental profile with a time-independent, cubic spline function based on the profile in the cross dispersion direction, with which we achieved a radial velocity precision similar to using a conventional "sum-of-Gaussians" instrumental profile: 1.8 m s1^{-1} over 1.5 months on the RV standard star HD 122064. Therefore, we conclude that the instrumental profile need not be perfectly accurate as long as it is stable. In addition, we observed 51 Peg and our results are consistent with the literature, confirming our spectrograph and Doppler pipeline are producing accurate and precise radial velocities.Comment: 22 pages, 9 figures, submitted to PASP, Peer-Reviewed and Accepte

    Measurement of the Branching Fraction for B- --> D0 K*-

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    We present a measurement of the branching fraction for the decay B- --> D0 K*- using a sample of approximately 86 million BBbar pairs collected by the BaBar detector from e+e- collisions near the Y(4S) resonance. The D0 is detected through its decays to K- pi+, K- pi+ pi0 and K- pi+ pi- pi+, and the K*- through its decay to K0S pi-. We measure the branching fraction to be B.F.(B- --> D0 K*-)= (6.3 +/- 0.7(stat.) +/- 0.5(syst.)) x 10^{-4}.Comment: 7 pages, 1 postscript figure, submitted to Phys. Rev. D (Rapid Communications
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