98 research outputs found

    Pre-Hawking Radiation from a Collapsing Shell

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    We investigate the effect of induced massive radiation given off during the time of collapse of a massive spherically symmetric domain wall in the context of the functional Schr\"odinger formalism. Here we find that the introduction of mass suppresses the occupation number in the infrared regime of the induced radiation during the collapse. The suppression factor is found to be given by eβme^{-\beta m}, which is in agreement with the expected Planckian distribution of induced radiation. Thus a massive collapsing domain wall will radiate mostly (if not exclusively) massless scalar fields, making it difficult for the domain wall to shed any global quantum numbers and evaporate before the horizon is formed.Comment: 10 pages, 3 figures. We updated the acknowledgments as well as added a statement clarifying that we are following the methods first laid out in Phys. Rev. D 76, 024005 (2007

    Measurement of the Mass Splittings between the bbˉχb,J(1P)b\bar{b}\chi_{b,J}(1P) States

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    We present new measurements of photon energies and branching fractions for the radiative transitions: Upsilon(2S)->gamma+chi_b(J=0,1,2). The masses of the chi_b states are determined from the measured radiative photon energies. The ratio of mass splittings between the chi_b substates, r==(M[J=2]-M[J=1])/(M[J=1]-M[J=0]) with M the chi_b mass, provides information on the nature of the bbbar confining potential. We find r(1P)=0.54+/-0.02+/-0.02. This value is in conflict with the previous world average, but more consistent with the theoretical expectation that r(1P)<r(2P); i.e., that this mass splittings ratio is smaller for the chi_b(1P) triplet than for the chi_b(2P) triplet.Comment: 11 page postscript file, postscript file also available through http://w4.lns.cornell.edu/public/CLN

    Radiative Decay Modes of the D0D^{0} Meson

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    Using data recorded by the CLEO-II detector at CESR we have searched for four radiative decay modes of the D0D^0 meson: D0ϕγD^0\to\phi\gamma, D0ωγD^0\to\omega\gamma, D0KˉγD^0\to\bar{K}^{*}\gamma, and D0ρ0γD^0\to\rho^0\gamma. We obtain 90% CL upper limits on the branching ratios of these modes of 1.9×1041.9\times 10^{-4}, 2.4×1042.4\times 10^{-4}, 7.6×1047.6\times 10^{-4} and 2.4×1042.4\times 10^{-4} respectively.Comment: 15 page postscript file, postscript file also available through http://w4.lns.cornell.edu/public/CLN

    An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

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    For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

    Driver Fusions and Their Implications in the Development and Treatment of Human Cancers.

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    Gene fusions represent an important class of somatic alterations in cancer. We systematically investigated fusions in 9,624 tumors across 33 cancer types using multiple fusion calling tools. We identified a total of 25,664 fusions, with a 63% validation rate. Integration of gene expression, copy number, and fusion annotation data revealed that fusions involving oncogenes tend to exhibit increased expression, whereas fusions involving tumor suppressors have the opposite effect. For fusions involving kinases, we found 1,275 with an intact kinase domain, the proportion of which varied significantly across cancer types. Our study suggests that fusions drive the development of 16.5% of cancer cases and function as the sole driver in more than 1% of them. Finally, we identified druggable fusions involving genes such as TMPRSS2, RET, FGFR3, ALK, and ESR1 in 6.0% of cases, and we predicted immunogenic peptides, suggesting that fusions may provide leads for targeted drug and immune therapy
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